Journal articles on the topic 'Arteriole'
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1
Boegehold, M. A. "Effect of dietary salt on arteriolar nitric oxide in striated muscle of normotensive rats." American Journal of Physiology-Heart and Circulatory Physiology 264, no. 6 (June 1, 1993): H1810—H1816. http://dx.doi.org/10.1152/ajpheart.1993.264.6.h1810.
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This study evaluated the influence of high dietary salt intake on nitric oxide (NO) activity in the arteriolar network of rats resistant to salt-induced hypertension. The spinotrapezius muscle microvasculature was studied in inbred Dahl salt-resistant (SR/Jr) rats fed low (0.45%)- or high (7%)-salt diets for 4–5 wk. Arterial pressures were not different between groups at any time during the study. NO synthesis inhibition with NG-nitro-L-arginine-methyl ester (L-NAME) constricted arcade arterioles in low-salt SR/Jr and dilated arcade arterioles in high-salt SR/Jr. Arcade arteriole dilation to acetylcholine (ACh), but not sodium nitroprusside (SNP), was impaired in high-salt SR/Jr. In contrast, transverse and distal arteriole responses to L-NAME, ACh, and SNP were identical in high- and low-salt SR/Jr. These findings indicate that high salt intake, in the absence of increased arterial pressure, suppresses the influence of basal and evoked NO on vascular tone in arcading arterioles, but not in smaller transverse and distal arterioles. Unaltered SNP responses in high-salt SR/Jr suggest that this effect does not involve a change in arteriolar smooth muscle responsiveness to NO.
2
Hester, R. L. "Venular-arteriolar diffusion of adenosine in hamster cremaster microcirculation." American Journal of Physiology-Heart and Circulatory Physiology 258, no. 6 (June 1, 1990): H1918—H1924. http://dx.doi.org/10.1152/ajpheart.1990.258.6.h1918.
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During increases in blood flow, both the terminal and the proximal arterioles dilate. The mechanism behind the dilation of the proximal arterioles is not known but may be the result of the diffusion of a vasoactive metabolite from adjacent venules. To determine whether an increase in venous adenosine (ADO) concentration could affect an adjacent arteriole, venules were perfused using a micropipette containing 10(-7)-10(-4) M ADO. During the venular perfusion, arteriolar diameter and red blood cell velocity were measured at a site 0.5 to 6 mm from the micropipette tip. The adjacent arteriole of the venular arteriolar pair dilated 29 +/- 3% with a 5-s 10(-4) M ADO perfusion, 32 +/- 4% with a 10-s 10(-4) M ADO perfusion, and 85 +/- 22% with a 60-s 10(-4) M ADO perfusion. One and 2-min perfusions with 10(-5) M ADO resulted in a 36 +/- 6% and 33 +/- 4% increase in diameter of the paired arteriole, respectively. The red blood cell velocity responses were variable, yet, on average, calculated blood flow increased in each group of experiments. Venular perfusions with saline resulted in a 2% change in arteriolar diameter. To rule out nondiffusional effects, venular perfusions were performed when the arteriole was not paired with the venule but crossed the venule. Venular perfusion with 10(-6) and 10(-7) M ADO resulted in a significant increase in diameter of the crossing arteriole of 19 +/- 3% and 6 +/- 2%, respectively. Therefore, the diffusion of a vasoactive metabolite from a venule to an arteriole may provide a mechanism by which the tissue can send a signal to cause a dilation of the more proximal arterioles.
3
Cohen, Kenneth D., Bradley R. Berg, and Ingrid H. Sarelius. "Remote arteriolar dilations in response to muscle contraction under capillaries." American Journal of Physiology-Heart and Circulatory Physiology 278, no. 6 (June 1, 2000): H1916—H1923. http://dx.doi.org/10.1152/ajpheart.2000.278.6.h1916.
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In hamster cremaster muscle, it has been shown previously that contraction of skeletal muscle fibers underlying small groups of capillaries (modules) induces dilations that are proportional to metabolic rate in the two arteriolar generations upstream of the stimulated capillaries (Berg BR, Cohen KD, and Sarelius IH. Am J Physiol Heart Circ Physiol 272: H2693–H2700, 1997). These remote dilations were hypothesized to be transmitted via gap junctions and not perivascular nerves. In the present study, halothane (0.07%) blocked dilation in the module inflow arteriole, and dilation in the second arteriolar generation upstream, the branch arteriole, was blocked by both 600 mosM sucrose and halothane but not tetrodotoxin (2 μM). Dilations in both arterioles were not blocked by the gap junction uncoupler 18-β-glycyrrhetinic acid (40 μM), and 80 mM KCl did not block dilation of the module inflow arteriole. These data implicate a gap junctional-mediated pathway insensitive to 18-β-glycyrrhetinic acid in dilating the two arterioles upstream of the capillary module during “remote” muscle contraction. Dilation in the branch arteriole, but not the module inflow arteriole, was attenuated by 100 μM N ω-nitro-l-arginine. Thus selective contraction of muscle fibers underneath capillaries results in dilations in the upstream arterioles that have characteristics consistent with a signal that is transmitted along the vessel wall through gap junctions, i.e., a conducted vasodilation. The observed insensitivities to 18-β-glycyrrhetinic acid, to KCl, and to N ω-nitro-l-arginine suggest, however, that there are multiple signaling pathways by which remote dilations can be initiated in these microvessels.
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Dawson, C. A., R. L. Capen, L. P. Latham, W. L. Hanson, S. E. Hofmeister, T. A. Bronikowski, D. A. Rickaby, and W. W. Wagner. "Pulmonary arterial transit times." Journal of Applied Physiology 63, no. 2 (August 1, 1987): 770–77. http://dx.doi.org/10.1152/jappl.1987.63.2.770.
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To begin to characterize the pulmonary arterial transport function we rapidly injected a bolus containing a radiopaque dye and a fluorescence dye into the right atrium of anesthetized dogs. The concentrations of the dye indicators were measured in the main pulmonary artery (fluoroscopically) and in a subpleural pulmonary arteriole (by fluorescence microscopy). The resulting concentration vs. time curves were subjected to numerical deconvolution and moment analysis to determine how the bolus was dispersed as it traveled through the arteriole stream tube from the main pulmonary artery to the arteriole. The mean transit time and standard deviation of the transport function from the main pulmonary artery to the arterioles studied averaged 1.94 and 1.23 s, respectively, and the relative dispersion (ratio of standard deviation to mean transit time) was approximately 64%. This relative dispersion is at least as large as those reported for the whole dog lung, indicating that relative to their respective mean transit times the dispersion upstream from the arterioles is comparable to that taking place in capillaries and/or veins. The standard deviations of the transport functions were proportional to their mean transit times. Thus the relative dispersion from the main pulmonary artery to the various arterioles studied was fairly consistent. However, there were variations in mean transit time even between closely adjacent arterioles, suggesting that variations in mean transit times between arteriole stream tubes also contribute to the dispersion in the pulmonary arterial tree.
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Park, Sungmi, Benjamin J. Bivona, and Lisa M. Harrison-Bernard. "Lack of contribution of nitric oxide synthase to cholinergic vasodilation in murine renal afferent arterioles." American Journal of Physiology-Renal Physiology 314, no. 6 (June 1, 2018): F1197—F1204. http://dx.doi.org/10.1152/ajprenal.00433.2017.
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We have previously reported significant increases in neuronal nitric oxide synthase (NOS) immunostaining in renal arterioles of angiotensin type 1A receptor (AT1A) knockout mice, and in arterioles and macula densa cells of AT1A/AT1B knockout mice. The contribution of nitric oxide derived from endothelial and macula densa cells in the maintenance of afferent arteriolar tone and acetylcholine-induced vasodilation was functionally determined in kidneys of wild-type, AT1A, and AT1A/AT1B knockout mice. Acetylcholine-induced changes in arteriolar diameters of in vitro blood-perfused juxtamedullary nephrons were measured during control conditions, in the presence of the nonspecific NOS inhibitor, Nω-nitro-l-arginine methyl ester (NLA), or the highly selective neuronal NOS inhibitor, N5-(1-imino-3-butenyl)-l-ornithine (VNIO). Acetylcholine (0.1 mM) produced a significant vasoconstriction in afferent arterioles of AT1A/AT1B mice (−10.9 ± 5.1%) and no changes in afferent arteriolar diameters of AT1A knockout mice. NLA (0.01–1 mM) or VNIO (0.01–1 μM) induced significant dose-dependent vasoconstrictions (−19.8 ± 4.0% 1 mM NLA; −7.8 ± 3.5% 1 μM VNIO) in afferent arterioles of kidneys of wild-type mice. VNIO had no effect on afferent arteriole diameters of AT1A knockout or AT1A/AT1B knockout mice, suggesting nonfunctional neuronal nitric oxide synthase. These data indicate that acetylcholine produces a significant renal afferent arteriole vasodilation independently of nitric oxide synthases in wild-type mice. AT1A receptors are essential for the manifestation of renal afferent arteriole responses to neuronal nitric oxide synthase-mediated nitric oxide release.
6
Baker, Wesley B., Ashwin B. Parthasarathy, Kimberly P. Gannon, Venkaiah C. Kavuri, David R. Busch, Kenneth Abramson, Lian He, et al. "Noninvasive optical monitoring of critical closing pressure and arteriole compliance in human subjects." Journal of Cerebral Blood Flow & Metabolism 37, no. 8 (May 25, 2017): 2691–705. http://dx.doi.org/10.1177/0271678x17709166.
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The critical closing pressure ( CrCP) of the cerebral circulation depends on both tissue intracranial pressure and vasomotor tone. CrCP defines the arterial blood pressure ( ABP) at which cerebral blood flow approaches zero, and their difference ( ABP − CrCP) is an accurate estimate of cerebral perfusion pressure. Here we demonstrate a novel non-invasive technique for continuous monitoring of CrCP at the bedside. The methodology combines optical diffuse correlation spectroscopy (DCS) measurements of pulsatile cerebral blood flow in arterioles with concurrent ABP data during the cardiac cycle. Together, the two waveforms permit calculation of CrCP via the two-compartment Windkessel model for flow in the cerebral arterioles. Measurements of CrCP by optics (DCS) and transcranial Doppler ultrasound (TCD) were carried out in 18 healthy adults; they demonstrated good agreement (R = 0.66, slope = 1.14 ± 0.23) with means of 11.1 ± 5.0 and 13.0 ± 7.5 mmHg, respectively. Additionally, a potentially useful and rarely measured arteriole compliance parameter was derived from the phase difference between ABP and DCS arteriole blood flow waveforms. The measurements provide evidence that DCS signals originate predominantly from arteriole blood flow and are well suited for long-term continuous monitoring of CrCP and assessment of arteriole compliance in the clinic.
7
Nurkiewicz, Timothy R., and Matthew A. Boegehold. "High dietary salt alters arteriolar myogenic responsiveness in normotensive and hypertensive rats." American Journal of Physiology-Heart and Circulatory Physiology 275, no. 6 (December 1, 1998): H2095—H2104. http://dx.doi.org/10.1152/ajpheart.1998.275.6.h2095.
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We evaluated arteriolar myogenic responsiveness in normotensive, salt-loaded and hypertensive rats and investigated the potential influence of luminal blood flow or shear stress on myogenic responses under each of these conditions. Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) fed low-salt (0.45%, LS) or high-salt (7%, HS) diets were enclosed in a ventilated airtight box with the spinotrapezius muscle exteriorized for intravital microscopy. Dietary salt did not affect mean arterial pressure (MAP) in WKY, whereas MAP in SHR was significantly higher and augmented by dietary salt. In all groups, box pressurization caused similar increases in MAP that were completely transmitted to the arterioles. After these pressure increases, large arteriole diameters decreased by 0–30% and intermediate arteriole diameters decreased by 21–27%. Arteriolar myogenic responsiveness was not different between WKY-LS and SHR-LS. Large arterioles in WKY-HS displayed an attenuated pressure-diameter relationship compared with that in WKY-LS. Large arterioles in SHR-HS displayed an augmented pressure-diameter relationship compared with that in SHR-LS. There were no correlations between resting flow or wall shear rate and the magnitude of initial myogenic constriction in any group or vessel type. The capacity for sustained myogenic constriction was unrelated to secondary decreases in flow (14–41%) or increases in wall shear rate (21–88%) in each group. We conclude that 1) dietary salt impairs the myogenic responsiveness of large arterioles in normotensive rats and augments the myogenic responsiveness of large arterioles in hypertensive rats, 2) hypertension does not alter arteriolar myogenic responsiveness in this vascular bed, and 3) flow- or shear-dependent mechanisms do not attenuate myogenic responses in the intact arteriolar network of normal, salt-loaded, or hypertensive rats.
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Kavdia, Mahendra, and Aleksander S. Popel. "Venular endothelium-derived NO can affect paired arteriole: a computational model." American Journal of Physiology-Heart and Circulatory Physiology 290, no. 2 (February 2006): H716—H723. http://dx.doi.org/10.1152/ajpheart.00776.2005.
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Venular endothelial cells can release nitric oxide (NO) in response to intraluminal flow both in isolated venules and in vivo. Experimental studies suggest that venular endothelium-released NO causes dilation of the adjacent paired arteriole. In the vascular wall, NO stimulates its target hemoprotein, soluble guanylate cyclase (sGC), which relaxes smooth muscle cells. In this study, a computational model of NO transport for an arteriole and venule pair was developed to determine the importance of the venular endothelium-released NO and its transport to the adjacent arteriole in the tissue. The model predicts that the tissue NO levels are affected within a wide range of parameters, including NO-red blood cell reaction rate and NO production rate in the arteriole and venule. The results predict that changes in the venular NO production affected not only venular endothelial and smooth muscle NO concentration but also endothelial and smooth muscle NO concentration in the adjacent arteriole. This suggests that the anatomy of microvascular tissue can permit the transport of NO from arteriolar to venular side, and vice versa, and may provide a mechanism for dilation of proximal arterioles by venules. These results will have significant implications for our understanding of tissue NO levels in both physiological and pathophysiological conditions.
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Mitrophanov, Alexander Y., Glenn Merrill-Skoloff, Steven P. Grover, Vijay Govindarajan, Arun Kolanjiyil, Daniel S. Hariprasad, Ginu Unnikrishnan, Robert Flaumenhaft, and Jaques Reifman. "Injury Length and Arteriole Constriction Shape Clot Growth and Blood-Flow Acceleration in a Mouse Model of Thrombosis." Arteriosclerosis, Thrombosis, and Vascular Biology 40, no. 9 (September 2020): 2114–26. http://dx.doi.org/10.1161/atvbaha.120.314786.
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Objective: Quantitative relationships between the extent of injury and thrombus formation in vivo are not well understood. Moreover, it has not been investigated how increased injury severity translates to blood-flow modulation. Here, we investigated interconnections between injury length, clot growth, and blood flow in a mouse model of laser-induced thrombosis. Approach and Results: Using intravital microscopy, we analyzed 59 clotting events collected from the cremaster arteriole of 14 adult mice. We regarded injury length as a measure of injury severity. The injury caused transient constriction upstream and downstream of the injury site resulting in a 50% reduction in arteriole diameter. The amount of platelet accumulation and fibrin formation did not depend on arteriole diameter or deformation but displayed an exponentially increasing dependence on injury length. The height of the platelet clot depended linearly on injury length and the arteriole diameter. Upstream arteriolar constriction correlated with delayed upstream velocity increase, which, in turn, determined downstream velocity. Before clot formation, flow velocity positively correlated with the arteriole diameter. After the onset of thrombus growth, flow velocity at the injury site negatively correlated with the arteriole diameter and with the size of the above-clot lumen. Conclusions: Injury severity increased platelet accumulation and fibrin formation in a persistently steep fashion and, together with arteriole diameter, defined clot height. Arterial constriction and clot formation were characterized by a dynamic change in the blood flow, associated with increased flow velocity.
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Kimura, K., Y. Hirata, S. Nanba, A. Tojo, H. Matsuoka, and T. Sugimoto. "Effects of atrial natriuretic peptide on renal arterioles: morphometric analysis using microvascular casts." American Journal of Physiology-Renal Physiology 259, no. 6 (December 1, 1990): F936—F944. http://dx.doi.org/10.1152/ajprenal.1990.259.6.f936.
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In normal rat kidneys, the effect of atrial natriuretic peptide (ANP) on the diameter of the arterioles was evaluated by scanning electron microscopy of vascular casts. Acryl resin was infused into rat kidneys during the administration of ANP, either alone or with norepinephrine (NE). ANP infusion constricted the proximal efferent arteriole in the superficial cortex. Although NE constricted the proximal and distal segments of the afferent arteriole in the superficial cortex, the addition of ANP reversed the constriction and further constricted the efferent arteriole. In the deep cortex, only the proximal segment of the afferent arteriole was dilated by ANP when infused with NE. In a separate set of experiments, ANP increased both the glomerular filtration rate (GFR) and urinary sodium excretion (UNaV), and NE decreased the renal blood flow (RBF). However, administration of ANP after NE recovered RBF and increased GFR as well as UNaV. Results indicate that ANP increases GFR and natriuresis by constricting the efferent arteriole. NE appears to decrease RBF by constricting the afferent arteriole. ANP antagonizes the renal effects of NE primarily by dilating afferent arterioles.
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Falcone, J. C., and H. G. Bohlen. "EDRF from rat intestine and skeletal muscle venules causes dilation of arterioles." American Journal of Physiology-Heart and Circulatory Physiology 258, no. 5 (May 1, 1990): H1515—H1523. http://dx.doi.org/10.1152/ajpheart.1990.258.5.h1515.
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Communication from venules to arterioles through the release of endothelial-derived relaxing factor (EDRF) was evaluated. To demonstrate that the rat intestinal and the spinotrapezius muscle arterioles can respond to EDRF, the vessels were dilated by iontophoretically applied acetylcholine (ACh), and this dilation was greatly attenuated by the inhibitors of EDRF actions, methylene blue (100 microM) and dithiothreitol (50 microM). The EDRF inhibitors did not suppress arteriolar dilation to typically applied adenosine (10(-4) M), an endothelium-independent dilator. Although ACh release onto the venular wall had minimal effects on the diameter of the venule, the paired arteriole would dilate 20-30% in the intestine and 50-60% in the spinotrapezius muscle. After EDRF inhibition, venular ACh exposure did not cause arteriolar dilation. ACh diffusion from venules to arterioles was not the cause of arteriolar dilation, because release of ACh into the tissue at the same distance as from the arteriole to the venular ACh release site caused minimal arteriolar dilation. Neither blockade of neural reflexes with tetrodotoxin (3 X 10(-6) M) nor suppression of prostaglandin formation with indomethacin (10(-5) M) prevented the arteriolar dilation during release of ACh onto the venular wall. The overall study indicated that communication from venules to arterioles through the release of EDRF from the venule did occur and caused substantial arteriolar vasodilation. Therefore circumstances within and around venules may influence regulation of nearby arterioles through an EDRF-mediated mechanism.
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Bai, Lun, Guangqian Wang, Xiaoyan Tan, and Jianmei Xu. "Exploring the Mechanism of Microarteriogenesis in Porous Silk Fibroin Film." International Journal of Biomaterials 2012 (2012): 1–6. http://dx.doi.org/10.1155/2012/262890.
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Purpose. Based on the experiment of the microarteriogenesis that is associated with angiogenesis during tissue repair process in porous silk fibroin films (PSFFs), we investigate the characteristics of micro-arteriogenesis and explore its mechanism.Methods. After the porous silk fibroin materials are implanted into the back hypodermal tissue of SD rats, the arteriole development and the morphogenesis of smooth muscle cell are histologically monitored and the micro-arteriogenesis is quantitatively analyzed.Results. 10 days after implantation, the arteriole density reaches the highest level in the junction of silk fibroin materials with tissues. Three weeks later, the arteriolar density in the materials reaches the maximum, and the arterioles in the junction of materials with tissues appear to be in a mature and upgrading state.Modeling of Microarteriogenesis. The arterioles in materials are generated after capillary angiogenesis. It is inferred that arteriolar development does not start until the network of the capillaries is formed. At first, the arterioles grow in the conjunct area of precapillaries with arterioles. Then with the extension of the arterioles, the upgrade of arterioles in connecting area is observed at a later stage. Based on the observation, the conditions and the mechanism of microarterializations as well as the upgrade of arterioles are analyzed.
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Reddi, V., A. Zaglul, E. S. Pentz, and R. A. Gomez. "Renin-expressing cells are associated with branching of the developing kidney vasculature." Journal of the American Society of Nephrology 9, no. 1 (January 1998): 63–71. http://dx.doi.org/10.1681/asn.v9163.
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To define the relationship between renal vascular development and renin distribution during kidney ontogeny, the complete renal arterial tree of Sprague Dawley rats during fetal (20 d) and postnatal (1 to 90 d) life was microdissected and immunostained for renin. A shift in renin distribution from interlobar and arcuate arteries in the fetus to the afferent arterioles in the adult was observed. In addition, seven types of renin distribution along the afferent arterioles were identified. In type I, renin was distributed continuously along the whole length of the afferent vessel. This pattern was most frequently observed in the fetus. In type II, renin extended upstream from the glomerulus but did not occupy the whole length of the arteriole. This type was relatively constant throughout postnatal life. In type III, renin was present as bands along the afferent vessel; it was most frequently observed in the fetal and early perinatal periods. In type IV, renin was restricted to the "classical" juxtaglomerular localization. It was the most frequent type observed in the adult rat. In type V, no renin was found in the arteriole. It was the second most frequent type observed in the adult rat. In addition, two "mixed" patterns, type III/IV and type III/II, were occasionally observed. The distribution of renin-expressing cells was spatially and temporally associated with the development of blood vessels. Development of a new arterial branch was preceded by the appearance of renin-expressing cells at the point of branching. This was followed by an outpouching of the arterial wall that progressively elongated to form a new arteriole. During this process, renin-expressing cells were distributed along the whole of the newly formed vessel. As the vessel matured, renin-expressing cells became restricted to the juxtaglomerular portion of the afferent arteriole. It is concluded that throughout life and within each individual arterial tree, expression of renin is heterogeneous, following patterns that are unique for each developmental stage. Furthermore, the association of renin-expressing cells with branching of renal arterioles suggests a role for these cells in the development of the kidney vasculature.
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Iddings, Jennifer A., Ki Jung Kim, Yiqiang Zhou, Haruki Higashimori, and Jessica A. Filosa. "Enhanced Parenchymal Arteriole Tone and Astrocyte Signaling Protect Neurovascular Coupling Mediated Parenchymal Arteriole Vasodilation in the Spontaneously Hypertensive Rat." Journal of Cerebral Blood Flow & Metabolism 35, no. 7 (March 11, 2015): 1127–36. http://dx.doi.org/10.1038/jcbfm.2015.31.
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Functional hyperemia is the regional increase in cerebral blood flow upon increases in neuronal activity which ensures that the metabolic demands of the neurons are met. Hypertension is known to impair the hyperemic response; however, the neurovascular coupling mechanisms by which this cerebrovascular dysfunction occurs have yet to be fully elucidated. To determine whether altered cortical parenchymal arteriole function or astrocyte signaling contribute to blunted neurovascular coupling in hypertension, we measured parenchymal arteriole reactivity and vascular smooth muscle cell Ca2+ dynamics in cortical brain slices from normotensive Wistar Kyoto (WKY) and spontaneously hypertensive (SHR) rats. We found that vasoconstriction in response to the thromboxane A2 receptor agonist U46619 and basal vascular smooth muscle cell Ca2+ oscillation frequency were significantly increased in parenchymal arterioles from SHR. In perfused and pressurized parenchymal arterioles, myogenic tone was significantly increased in SHR. Although K+-induced parenchymal arteriole dilations were similar in WKY and SHR, metabotropic glutamate receptor activation-induced parenchymal arteriole dilations were enhanced in SHR. Further, neuronal stimulation-evoked parenchymal arteriole dilations were similar in SHR and WKY. Our data indicate that neurovascular coupling is not impaired in SHR, at least at the level of the parenchymal arterioles.
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Smiesko, V., D. J. Lang, and P. C. Johnson. "Dilator response of rat mesenteric arcading arterioles to increased blood flow velocity." American Journal of Physiology-Heart and Circulatory Physiology 257, no. 6 (December 1, 1989): H1958—H1965. http://dx.doi.org/10.1152/ajpheart.1989.257.6.h1958.
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Arcading arterioles (average diam 68 microns ID) connecting adjacent triangular vascular sectors in the rat mesentery were examined in vivo for the presence of flow-dependent vasodilation. When a feed artery to one of these sectors was occluded, the affected sector was supplied by collateral flow through the arcading arteriole, and red cell velocity in the arteriole increased by 10-66 mm/s. The velocity increase was followed (with an average delay of 7.7 s) by dilation of the arcading arteriole, which averaged 68%. The dilation was closely correlated with red cell velocity (r = 0.96), volume flow (r = 0.96), and wall shear rate (r = 0.89). The dilation was sustained for the duration of increased velocity (1-10 min) and was not affected when direction of flow in the arteriole was reversed. The flow-induced dilation was equal to the maximal dilation attained with topically applied papaverine. Dilation of the arcading arteriole could be almost completely abolished if the arteriole was also occluded during occlusion of a feed artery. These observations indicate that a potent flow-dependent dilator mechanism is present in arcading arterioles of rat mesentery and may play an important role in local regulation.
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Hsu, R., and T. W. Secomb. "Analysis of Oxygen Exchange Between Arterioles and Surrounding Capillary-Perfused Tissue." Journal of Biomechanical Engineering 114, no. 2 (May 1, 1992): 227–31. http://dx.doi.org/10.1115/1.2891376.
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A theoretical model is used to analyze oxygen transport in a three-dimensional tissue region containing an arteriole surrounded by an array of capillaries in planes perpendicular to the arteriole. Convective removal of oxygen from the vicinity of the arteriole by nearby capillaries is shown to increase diffusive oxygen loss from the arteriole. This effect depends on the locations of the capillaries, particularly those nearest to the arteriole. The arteriolar oxygen efflux is comparable to that predicted by a previous model which used a continuum approach, but the efflux does not increase with increasing perfusion as rapidly as predicted by the continuum model. Even a small capillary flow rate strongly influences the oxygen field surrounding the arteriole.
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Hayashi, K., M. Epstein, R. Loutzenhiser, and H. Forster. "Impaired myogenic responsiveness of the afferent arteriole in streptozotocin-induced diabetic rats: role of eicosanoid derangements." Journal of the American Society of Nephrology 2, no. 11 (May 1992): 1578–86. http://dx.doi.org/10.1681/asn.v2111578.
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Evidence suggests that diabetes is associated with an impairment of renal autoregulation. It has previously been demonstrated that pressure-induced (myogenic) afferent arteriolar vasoconstriction is well preserved in the isolated perfused hydronephrotic kidney. In this study, pressure-induced afferent arteriolar vasoconstriction was examined in kidneys from streptozotocin-induced diabetic rats. Vessel diameters were measured by videomicroscopy as renal arterial pressure was elevated from 80 to 180 mm Hg. In normal kidneys, the afferent arteriole vasoconstricted progressively as renal arterial pressure was increased (-24 +/- 2% decrement in diameter at 180 mm Hg; N = 35; P less than 0.001). In contrast, afferent arterioles of diabetic kidneys exhibited a greatly attenuated response to pressure (i.e., -3 +/- 2% change at 180 mm Hg; N = 60). In vitro treatment with 100 microM ibuprofen completely restored myogenic vasoconstriction (-21 +/- 2% change at 180 mm Hg), but did not alter myogenic responses of control (i.e., nondiabetic) kidneys. The control of hyperglycemia by insulin treatment resulted in a partial preservation of myogenic vasoconstriction (i.e., -11 +/- 3% change at 180 mm Hg), which was further restored by the administration of a low dose (10 microM) of ibuprofen (-21 +/- 1% change at 180 mm Hg). These observations indicate that diabetes is associated with an impaired responsiveness of the afferent arteriole to pressure that is mediated by an alteration in eicosanoid metabolism. This deranged renal microcirculatory response to pressure may represent a functional impairment of the diabetic kidney that may contribute to the progression of diabetic nephropathy.
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Schnackenberg, Christine G., William J. Welch, and Christopher S. Wilcox. "TP receptor-mediated vasoconstriction in microperfused afferent arterioles: roles of O2 − and NO." American Journal of Physiology-Renal Physiology 279, no. 2 (August 1, 2000): F302—F308. http://dx.doi.org/10.1152/ajprenal.2000.279.2.f302.
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Thromboxane A2 (TxA2) preferentially constricts the renal afferent arteriole. Nitric oxide (NO) modulates vasoconstriction and is rapidly degraded by superoxide radical (O2 −). We investigated the roles of NO and O2 − in rabbit isolated, perfused renal afferent arteriole responses to the TxA2/prostaglandin H2 (TP) receptor agonist U-46,619. U-46,619 (10−10–10−6 M) dose-dependently reduced afferent arteriolar luminal diameter (ED50 = 7.5 ± 5.0 nM), which was blocked by the TP receptor antagonist ifetroban (10−6 M). Tempol (10−3 M) pretreatment, which prevented paraquat-induced vasoconstriction in afferent arterioles, blocked the vasoconstrictor responses to U-46,619. To test whether U-46,619 stimulates NO and whether tempol prevents U-46,619-induced vasoconstriction by enhancing the biological activity of NO, we examined the luminal diameter response to U-46,619 in arterioles pretreated with N w-nitro-l-arginine methyl ester (l-NAME, 10−4 M) or l-NAME + tempol. During l-NAME, the sensitivity and maximal responses of the afferent arteriole to U-46,619 were significantly ( P < 0.05) enhanced. Moreover, l-NAME restored a vasoconstrictor response to U-46,619 in vessels pretreated with tempol. In conclusion, in isolated perfused renal afferent arterioles TP receptor activation stimulates NO production, which buffers the vasoconstriction, and stimulates O2 −production, which mediates the vasoconstriction, in part, through interaction with NO.
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Fallet, Rachel W., Hideki Ikenaga, Joseph P. Bast, and Pamela K. Carmines. "Relative contributions of Ca2+ mobilization and influx in renal arteriolar contractile responses to arginine vasopressin." American Journal of Physiology-Renal Physiology 288, no. 3 (March 2005): F545—F551. http://dx.doi.org/10.1152/ajprenal.00150.2002.
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Experiments addressed the hypothesis that afferent and efferent arterioles differentially rely on Ca2+ influx and/or release from intracellular stores in generating contractile responses to AVP. The effect of Ca2+ store depletion or voltage-gated Ca2+ channel (VGCC) blockade on contractile responsiveness to AVP (0.01–1.0 nM) was assessed in blood-perfused juxtamedullary nephrons from rat kidney. Depletion of intracellular Ca2+ stores by 100 μM cyclopiazonic acid (CPA) or 1 μM thapsigargin treatment increased afferent arteriolar baseline diameter by 14 and 21%, respectively, but did not significantly alter efferent arteriolar diameter. CPA attenuated the contractile response to 1.0 nM AVP by 34 and 55% in afferent and efferent arterioles, respectively ( P = 0.013). The impact of thapsigargin on AVP-induced afferent arteriolar contraction (52% inhibition) was also less than its effect on the efferent arteriolar response (88% inhibition; P = 0.046). In experiments probing the role of the Ca2+ influx through VGCCs, 10 μM diltiazem evoked a 34% increase in baseline afferent arteriolar diameter and attenuated the contractile response to 1.0 nM AVP by 45%, without significantly altering efferent arteriolar baseline diameter or responsiveness to AVP. Combined treatment with both diltiazem and thapsigargin prevented AVP-induced contraction of both vascular segments. We conclude that Ca2+ release from the intracellular stores contributes to the contractile response to AVP in both afferent and efferent arterioles but is more prominent in the efferent arteriole. Moreover, the VGCC contribution to AVP-induced renal arteriolar contraction resides primarily in the afferent arteriole.
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Busija, D. W., and J. Chen. "Reversal by increased CSF [H+] and [K+] of phorbol ester-induced arteriolar constriction in piglets." American Journal of Physiology-Heart and Circulatory Physiology 263, no. 5 (November 1, 1992): H1455—H1459. http://dx.doi.org/10.1152/ajpheart.1992.263.5.h1455.
Full textAbstract:
We determined whether several dilator stimuli could counteract phorbol ester-induced constriction of pial arterioles. A closed cranial window was implanted, and the diameter of one pial arteriole was determined by intravital microscopy in newborn pigs. Diameter of one pial arteriole was determined during baseline conditions and topical application of 10(-5) M phorbol 12, 13-dibutyrate (PDB) and during subsequent application of one of the following: arterial hypercapnia (inhalation of 10% CO2), topical application of cerebrospinal fluid with 12 mM K+, or topical application of 10(-5) M isoproterenol in cerebrospinal fluid. PDB constricted the arterioles from 101 +/- 5 to 70 +/- 5 microns (27 +/- 4%; n = 28). During this period of constriction which lasted longer than subsequent interventions (> 90 min), arterial hypercapnia dilated the arterioles by 85 +/- 19% (n = 12), and topical 12 mM K+ dilated the arterioles by 59 +/- 12% and caused vasomotion (n = 7). Despite blockade of direct dilator effects of arterial hypercapnia by indomethacin, arterial hypercapnia still reversed phorbol ester-induced constriction, suggesting that acidosis by itself is sufficient to cause this effect. In contrast, topical isoproterenol did not dilate PDB-constricted arterioles (n = 9); however, topical forskolin (2.4 x 10(-7) M) did reverse constriction, implying that protein kinase C activation may interfere with proper functioning of the beta-adrenoceptor. Therefore, increased extracellular fluid levels of K+ and H+, but not isoproterenol, are able to interfere with cerebrovascular consequences of protein kinase C activation.
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Nishimura, Nozomi, Nathanael L. Rosidi, Costantino Iadecola, and Chris B. Schaffer. "Limitations of Collateral Flow after Occlusion of a Single Cortical Penetrating Arteriole." Journal of Cerebral Blood Flow & Metabolism 30, no. 12 (September 15, 2010): 1914–27. http://dx.doi.org/10.1038/jcbfm.2010.157.
Full textAbstract:
Occlusions of penetrating arterioles, which plunge into cortex and feed capillary beds, cause severe decreases in blood flow and are potential causes of ischemic microlesions. However, surrounding arterioles and capillary beds remain flowing and might provide collateral flow around the occlusion. We used femtosecond laser ablation to trigger clotting in single penetrating arterioles in rat cortex and two-photon microscopy to measure changes in microvessel diameter and red blood cell speed after the clot. We found that after occlusion of a single penetrating arteriole, nearby penetrating and surface arterioles did not dilate, suggesting that alternate blood flow routes are not actively recruited. In contrast, capillaries showed two types of reactions. Capillaries directly downstream from the occluded arteriole dilated after the clot, but other capillaries in the same vicinity did not dilate. This heterogeneity in capillary response suggests that signals for vasodilation are vascular rather than parenchymal in origin. Although both neighboring arterioles and capillaries dilated in response to topically applied acetylcholine after the occlusion, the flow in the territory of the occluded arteriole did not improve. Collateral flow from neighboring penetrating arterioles is neither actively recruited nor effective in improving blood flow after the occlusion of a single penetrating arteriole.
22
Lubbe, A. S., R. N. Garrison, H. M. Cryer, N. L. Alsip, and P. D. Harris. "EDRF as a possible mediator of sepsis-induced arteriolar dilation in skeletal muscle." American Journal of Physiology-Heart and Circulatory Physiology 262, no. 3 (March 1, 1992): H880—H887. http://dx.doi.org/10.1152/ajpheart.1992.262.3.h880.
Full textAbstract:
Vascular endothelial cells influence microvessel diameters in vivo and in vitro and participate in host-defense mechanisms during sepsis. We examined whether small arteriole dilation in skeletal muscle during high cardiac output bacteremia (HOB) and low cardiac output live Escherichia coli sepsis (LOS) is mediated by an endothelium-derived relaxing factor (EDRF). Local chemical blockade of EDRF by hydroquinone (HQ) substantially blunted acetylcholine-induced dilation of small arterioles. HQ also prevented large arteriole (55-135 microns) constriction and small arteriole (6-22 microns) dilation in the cremaster muscle of rats during HOB. In LOS, small arteriole dilation was also prevented by HQ but only during the early period when blood pressure was unchanged from baseline. HQ did not alter large arteriole constriction during LOS. We conclude that small arteriole vasodilation in skeletal muscle is mediated at least in part by EDRF during bacteremia. Because EDRF cannot mediate large arteriole constriction and because HQ blunted large arteriole constriction during HOB, we now suspect that HQ also interferes at least in part with some large arteriole vasoconstrictor mechanism, possibly leukotrienes or an endothelium-derived constricting factor, which mediates large arteriole constriction during HOB. Our data also suggest that large arteriole constriction during LOS is partly mediated by factors that are unaffected by HQ. The endothelium appears to play an important role in the microcirculatory responses of skeletal muscle to live E. coli sepsis through more than one mechanism.
23
Segal, S. S. "Microvascular recruitment in hamster striated muscle: role for conducted vasodilation." American Journal of Physiology-Heart and Circulatory Physiology 261, no. 1 (July 1, 1991): H181—H189. http://dx.doi.org/10.1152/ajpheart.1991.261.1.h181.
Full textAbstract:
The influence of conducted vasodilation upon arteriolar diameter and capillary red blood cell (rbc) perfusion was investigated in the cremaster muscle of male hamsters anesthetized with pentobarbital. The muscle was surgically exposed, superfused with physiological saline solution (pH 7.4; 34 degrees C), and transilluminated for observation of microvessels using intravital video microscopy. The tip (2 microns ID) of a glass micropipette filled with acetylcholine (ACh; 1.0 M) was positioned adjacent to an arteriole. Microiontophoretic delivery of an ACh stimulus (200-1,000 nA; 200-750 ms) caused vasodilation at the pipette tip, which conducted rapidly along the arteriole and decayed with distance; this was characterized by length constants of 2.1 and 2.4 mm (P greater than 0.05) for arterioles with maximal diameters of 32 +/- 2 (means +/- SE; n = 8) and 63 +/- 2 microns (n = 5), respectively. When applied to the distal end of a terminal arteriole (TA) devoid of flow, ACh triggered a dilation that was conducted proximally (greater than 1,000 microns upstream) into the parent vessel (terminal arteriole feed, TAF) containing rbc flow, thereby inducing flow into the TA; stimulation of the TAF also induced rbc flow into TA. In capillaries fed by TA, rbc flux (rbc/s) increased from zero at rest to 23 +/- 6 during the peak of the TA dilation (n = 9); calculated tube hematocrit increased from 4 +/- 2 to 28 +/- 3%. Findings demonstrate that conduction of vasodilation can coordinate vasomotor responses between terminal and parent arterioles and promote rbc delivery to capillaries supplying striated muscle fibers.
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Loutzenhiser, R., K. Hayashi, and M. Epstein. "Divergent effects of KCl-induced depolarization on afferent and efferent arterioles." American Journal of Physiology-Renal Physiology 257, no. 4 (October 1, 1989): F561—F564. http://dx.doi.org/10.1152/ajprenal.1989.257.4.f561.
Full textAbstract:
We have previously proposed that renal microvessels exhibit a unique regional heterogeneity. Studies with calcium channel agonists and antagonists suggest that potential-dependent calcium channels may play a more prominent role in the activation of the afferent arteriole than the efferent arteriole. Because KCl-induced depolarization elicits vasoconstriction exclusively by the activation of potential-dependent calcium channels, we tested this postulate directly by ascertaining the vasoconstrictor effects of KCl and countervailing effects of a calcium channel blocker on the afferent and efferent arteriole of isolated perfused hydronephrotic kidneys. Increasing media potassium concentration from 5 to 30 mM resulted in a marked renal vasoconstriction decreasing renal perfusate flow by 61 +/- 4%. An examination of the microvascular response to KCl revealed a predominant response of the afferent arteriole. Thus afferent arteriolar diameter decreased by 38 +/- 6% (i.e., from 20.7 +/- 1.5 to 13.0 +/- 1.8 microns, P less than 0.005), whereas efferent arteriolar diameter decreased by only 12 +/- 4% (i.e., from 15.8 +/- 1.6 to 13.8 +/- 1.4 microns, P = 0.05). Nifedipine completely returned afferent arteriolar diameter to control levels with a mean effective dose of 41 +/- 2 nM. These findings indicate that the afferent arteriole is more responsive to depolarization-induced vasoconstrictor stimuli than is the efferent arteriole and suggest a greater prevalence of potential-dependent calcium channels in this vessel.
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McGahren, E. D., K. A. Dora, D. N. Damon, and B. R. Duling. "A test of the role of flow-dependent dilation in arteriolar responses to occlusion." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 2 (February 1, 1997): H714—H721. http://dx.doi.org/10.1152/ajpheart.1997.272.2.h714.
Full textAbstract:
At an arteriolar bifurcation, occlusion of one of the branch arterioles has been reported to result in an increase in flow, shear stress, and vasodilation in the opposite unoccluded branch. This dilator response in the unoccluded branch, often referred to as the "parallel occlusion response," has been cited as evidence that flow-dependent dilation is a primary regulator of arteriolar diameter in the microcirculation. It has not been previously noted that, during this maneuver, flow through the feed arteriole would be expected to decrease and logically should cause that vessel to constrict. We tested this prediction in vivo by measuring red blood cell (RBC) velocity and diameter changes in response to arteriolar occlusion in the microcirculatory beds of three preparations: the hamster cheek pouch, the hamster cremaster, and the rat cremaster. In all preparations, a vasodilation was observed in the feed arteriole, despite a decrease in both flow and calculated wall shear stress through this vessel. Unexpectedly, we found that dilation occurred in the unoccluded branch arterioles even in those cases in which RBC velocity and shear stress did not increase in the unoccluded branch arterioles. All values returned to the baseline level after the removal of occlusion. The magnitude of the dilation of the feed and branch arterioles varied between species and tissues, but feed and branch arterioles within a given preparation always responded in a similar way to each other. We conclude from our experiments that mechanisms other than flow-dependent dilation are involved in the vasodilation observed in the microcirculation during occlusion of an arteriolar branch.
26
Xi, Qi, Edward Umstot, Guiling Zhao, Damodaran Narayanan, Charles W. Leffler, and Jonathan H. Jaggar. "Glutamate regulates Ca2+ signals in smooth muscle cells of newborn piglet brain slice arterioles through astrocyte- and heme oxygenase-dependent mechanisms." American Journal of Physiology-Heart and Circulatory Physiology 298, no. 2 (February 2010): H562—H569. http://dx.doi.org/10.1152/ajpheart.00823.2009.
Full textAbstract:
Glutamate is the principal cerebral excitatory neurotransmitter and dilates cerebral arterioles to match blood flow to neural activity. Arterial contractility is regulated by local and global Ca2+ signals that occur in smooth muscle cells, but modulation of these signals by glutamate is poorly understood. Here, using high-speed confocal imaging, we measured the Ca2+ signals that occur in arteriole smooth muscle cells of newborn piglet tangential brain slices, studied signal regulation by glutamate, and investigated the physiological function of heme oxygenase (HO) and carbon monoxide (CO) in these responses. Glutamate elevated Ca2+ spark frequency by ∼188% and reduced global intracellular Ca2+ concentration ([Ca2+]i) to ∼76% of control but did not alter Ca2+ wave frequency in brain arteriole smooth muscle cells. Isolation of cerebral arterioles from brain slices abolished glutamate-induced Ca2+ signal modulation. In slices treated with l-2-α-aminoadipic acid, a glial toxin, glutamate did not alter Ca2+ sparks or global [Ca2+]i but did activate Ca2+ waves. This shift in Ca2+ signal modulation by glutamate did not occur in slices treated with d-2-α-aminoadipic acid, an inactive isomer of l-2-α-aminoadipic acid. In the presence of chromium mesoporphyrin, a HO blocker, glutamate inhibited Ca2+ sparks and Ca2+ waves and did not alter global [Ca2+]i. In isolated arterioles, CORM-3 [tricarbonylchloro(glycinato)ruthenium(II)], a CO donor, activated Ca2+ sparks and reduced global [Ca2+]i. These effects were blocked by 1 H-(1,2,4)-oxadiazolo-(4,3-a)-quinoxalin-1-one, a soluble guanylyl cyclase inhibitor. Collectively, these data indicate that glutamate can modulate Ca2+ sparks, Ca2+ waves, and global [Ca2+]i in arteriole smooth muscle cells via mechanisms that require astrocytes and HO. These data also indicate that soluble guanylyl cyclase is involved in CO activation of Ca2+ sparks in arteriole smooth muscle cells.
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Loutzenhiser, R., L. Chilton, and G. Trottier. "Membrane potential measurements in renal afferent and efferent arterioles: actions of angiotensin II." American Journal of Physiology-Renal Physiology 273, no. 2 (August 1, 1997): F307—F314. http://dx.doi.org/10.1152/ajprenal.1997.273.2.f307.
Full textAbstract:
An adaptation of the in vitro perfused hydronephrotic rat kidney model allowing in situ measurement of arteriolar membrane potentials is described. At a renal perfusion pressure of 80 mmHg, resting membrane potentials of interlobular arteries (22 +/- 2 microns) and afferent (14 +/- 1 microns) and efferent arterioles (12 +/- 1 microns) were -40 +/- 2 (n = 8), -40 +/- 1 (n = 45), and -38 +/- 2 mV (n = 22), respectively (P = 0.75). Using a dual-pipette system to stabilize the impalement site, we measured afferent and efferent arteriolar membrane potentials during angiotensin II (ANG II)-induced vasoconstriction. ANG II (0.1 nM) reduced afferent arteriolar diameters from 13 +/- 1 to 8 +/- 1 microns (n = 8, P = 0.005) and membrane potentials from -40 +/- 2 to -29 +/- mV (P = 0.012). ANG II elicited a similar vasoconstriction in efferent arterioles, decreasing diameters from 13 +/- 1 to 8 +/- 1 microns (n = 8, P = 0.004), but failed to elicit a significant depolarization (-39 +/- 2 for control; -36 +/- 3 mV for ANG II; P = 0.27). Our findings thus indicate that resting membrane potentials of pre- and postglomerular arterioles are similar and lie near the threshold activation potential for L-type Ca channels. ANG II-induced vasoconstriction appears to be closely coupled to membrane depolarization in the afferent arteriole, whereas mechanical and electrical responses appear to be dissociated in the efferent arteriole.
28
Rivers, R. J., and B. R. Duling. "Arteriolar endothelial cell barrier separates two populations of muscarinic receptors." American Journal of Physiology-Heart and Circulatory Physiology 262, no. 4 (April 1, 1992): H1311—H1315. http://dx.doi.org/10.1152/ajpheart.1992.262.4.h1311.
Full textAbstract:
The endothelium of arterioles can function as a barrier to diffusion of hydrophilic molecules when studied in vitro. Thus a substance applied to one side of the arteriole is relatively ineffective in reaching receptors on the opposite side of the vessel wall unless it is lipid soluble. To study the receptor populations on the two sides of the arteriolar endothelium, we used micropipettes to apply methacholine (MCh; 1.0 microM), either luminally or adventitially, for 5 s to the arterioles of the cheek pouch of pentobarbital-anesthetized hamsters. MCh equally dilated the arterioles regardless of the side of application. That different populations of receptors are located on either side of the arteriole was shown by the fact that adventitially applied hydrophilic methscopolamine was ineffective in blocking the effects of the luminally applied MCh but completely blocked the effects of abluminally applied MCh. In contrast, the luminal population of receptors was easily blocked by adventially applied scopolamine, which is lipophilic. Separate and independent populations of receptors in the vessel wall suggests the potential for differential control between humoral and adventitial sources of vasoactive metabolites.
29
Honig, C. R., T. E. Gayeski, A. Clark, and P. A. Clark. "Arteriovenous oxygen diffusion shunt is negligible in resting and working gracilis muscles." American Journal of Physiology-Heart and Circulatory Physiology 261, no. 6 (December 1, 1991): H2031—H2043. http://dx.doi.org/10.1152/ajpheart.1991.261.6.h2031.
Full textAbstract:
Distribution of O2 within and among arterioles and venules was determined in dog and rat gracilis muscles with a cryospectrophotometric method. Saturation in 40-microns arterioles was not demonstrably different from saturation in the aorta even when flow was abnormally low. Arterioles greater than 40 microns ran parallel to venules. Measurements and a mathematical model indicate that diffusive shunting is negligible for typical separation distances between arterioles and venules. Most separation distances were greater than 30 microns. In some venule segments less than 15 microns from an arteriole, saturation within 10 microns of the wall facing the arteriole was higher than at other locations within the venule. However, saturation in the population of venules did not increase with venule diameter, and mean venular saturation was not different from saturation in effluent blood. We make the following conclusions: 1) a small arteriovenous diffusive O2 flux exists in postural muscles; 2) contribution of this flux to O2 mass balance is negligible; 3) O2 diffusivity of the arteriolar wall and surrounding tissue in vivo cannot be much higher than O2 diffusivity determined in vitro; and 4) effluent PO2 closely approximates mean end-capillary PO2.
30
Nagasaka, Y., M. Ishigaki, H. Okazaki, J. Huang, M. Matsuda, T. Noguchi, H. Toga, T. Fukunaga, S. Nakajima, and N. Ohya. "Effect of pulmonary blood flow on microvascular pressure profile determined by micropuncture in perfused cat lungs." Journal of Applied Physiology 77, no. 4 (October 1, 1994): 1834–39. http://dx.doi.org/10.1152/jappl.1994.77.4.1834.
Full textAbstract:
To clarify the role of the pulmonary microvasculature in adjusting to increased pulmonary blood flow, we measured arteriolar and venular pressure by the servo-null micropuncture method while changing the pulmonary blood flow in isolated perfused cat lungs. We divided the lung vasculature into three longitudinal segments: 1) arterial (pulmonary artery to 30- to 50-microns arteriole), 2) microvascular (between 30- to 50-microns arteriole and venule), and 3) venous (30- to 50-microns venule to left atrium). The vascular resistance was calculated by dividing the pressure gradient by the flow. The pressure gradient of the microvascular segment did not increase, whereas the pressure gradient of the arterial and venous segments increased simultaneously with flow rate. Total and microvascular resistance decreased with increase of flow rate. Resistances of the arterial and venous segments did not change with increase in flow. We conclude that the microvasculature plays a crucial role in preventing pulmonary hypertension with increases in flow by decreasing microvascular resistance.
31
Kaley, Akos Koller gabor. "Letters to the Editor." American Journal of Physiology-Heart and Circulatory Physiology 274, no. 1 (January 1, 1998): H382—H383. http://dx.doi.org/10.1152/ajpheart.1998.274.1.h382.
Full textAbstract:
The following is the abstract of the article discussed in the subsequent letter: McGahren, Eugene D., Kim A. Dora, David N. Damon, and Brian R. Duling. A test of the role of flow-dependent dilation in arteriolar responses to occlusion. Am. J. Physiol. 272 ( Heart Circ. Physiol. 41): H714–H721, 1997.—At an arteriolar bifurcation, occlusion of one of the branch arterioles has been reported to result in an increase in flow, shear stress, and vasodilation in the opposite unoccluded branch. This dilator response in the unoccluded branch, often referred to as the “parallel occlusion response,” has been cited as evidence that flow-dependent dilation is a primary regulator of arteriolar diameter in the microcirculation. It has not been previously noted that, during this maneuver, flow through the feed arteriole would be expected to decrease and logically should cause that vessel to constrict. We tested this prediction in vivo by measuring red blood cell (RBC) velocity and diameter changes in response to arteriolar occlusion in the microcirculatory beds of three preparations: the hamster cheek pouch, the hamster cremaster, and the rat cremaster. In all preparations, a vasodilation was observed in the feed arteriole, despite a decrease in both flow and calculated wall shear stress through this vessel. Unexpectedly, we found that dilation occurred in the unoccluded branch arterioles even in those cases in which RBC velocity and shear stress did not increase in the unoccluded branch arterioles. All values returned to the baseline level after the removal of occlusion. The magnitude of the dilation of the feed and branch arterioles varied between species and tissues, but feed and branch arterioles within a given preparation always responded in a similar way to each other. We conclude from our experiments that mechanisms other than flow-dependent dilation are involved in the vasodilation observed in the microcirculation during occlusion of an arteriolar branch.
32
Denton, K. M., P. A. Fennessy, D. Alcorn, and W. P. Anderson. "Morphometric analysis of the actions of angiotensin II on renal arterioles and glomeruli." American Journal of Physiology-Renal Physiology 262, no. 3 (March 1, 1992): F367—F372. http://dx.doi.org/10.1152/ajprenal.1992.262.3.f367.
Full textAbstract:
To study the effects of angiotensin II on afferent and efferent arteriole diameters and on intraglomerular dimensions, angiotensin II (20 ng.kg-1.min-1) or saline vehicle was infused intravenously for 20 min into anesthetized rabbits pretreated with enalapril. Both kidneys were perfusion fixed (glutaraldehyde), and vascular casts were made of the right kidneys using methacrylate. Morphometric analysis of the left kidneys using transmission electron microscopy revealed no significant effects of angiotensin II within the glomerulus, including the degree of mesangial contraction. The diameters of the afferent and efferent arteriole casts from the right kidneys were measured at 20, 50, and 75 microns from the glomerulus by scanning electron microscopy. In the outer cortex the mean diameters of the afferent and efferent arterioles were 14.1 +/- 0.8 and 9.7 +/- 0.5 microns, respectively, in the angiotensin II-infused rabbits, significantly less than in the control (vehicle) rabbits, 17.0 +/- 0.7 microns (P less than 0.001) and 10.7 +/- 0.4 microns (P less than 0.005), respectively. Calculation of the relative changes in vascular resistance, however, indicated that the effects of angiotensin II on efferent arteriole resistance (average difference 2.4 +/- 1.2 units/microns) were significantly greater per unit length than the effects on afferent arteriole resistance (average difference 0.9 +/- 0.3 units/microns). Thus infused angiotensin II caused greater reduction in afferent arteriolar diameter than in efferent, but the calculated increase in vascular resistance per micron was greater in efferent vessels due to their smaller resting diameter.
33
Snyder, GK, B. Gannon, and RV Baudinette. "Microvascular Geometry in the Brain of the Lizard Trachydosaurus-Rugosus." Australian Journal of Zoology 38, no. 4 (1990): 387. http://dx.doi.org/10.1071/zo9900387.
Full textAbstract:
The vasculature and microvasculature in the central nervous system of the lizard Trnchydosaurus rugosus was examined by means of scanning electron microscopy of vascular corrosion casts. The arterial supply to the brain is from paired internal carotids. Secondary branches from these feeder arteries form a network over the surface of the lizard brain, giving rise to artery-vein vessel pairs. The vessel pairs bend at right angles to the brain surface, giving rise to terminal arteriole-venular pairs which penetrate the brain substance. Capillaries arise at fairly regular intervals along the vessel pairs, each originating from the arteriole and terminating in the venule at a site contiguous with its origin from the arteriole. In this way all of the capillaries in the central nervous system of the lizard form countercurrent loops. Anastomotic connections between arteriole-venular pairs do not occur, each arterial vessel being an end artery.
34
Weihprecht, H., J. N. Lorenz, J. P. Briggs, and J. Schnermann. "Vasoconstrictor effect of angiotensin and vasopressin in isolated rabbit afferent arterioles." American Journal of Physiology-Renal Physiology 261, no. 2 (August 1, 1991): F273—F282. http://dx.doi.org/10.1152/ajprenal.1991.261.2.f273.
Full textAbstract:
The present studies were performed to examine the vasoconstrictor effect of angiotensin II (ANG II), angiotensin III (ANG III), and vasopressin in isolated afferent arterioles of the rabbit kidney. Afferent arterioles were dissected together with their glomerulus and perfused with a pressure head of 120 cmH2O. Changes in vasomotor tone were assessed as diameter changes on videotaped recordings. Afferent arterioles responded to the angiotensins and vasopressin with dose-dependent reductions in vascular diameters with half-maximum responses being observed at concentrations between 10(-9) and 10(-8) M. Responses to ANG II and III were inhibited by saralasin. Contractile responses to ANG II and vasopressin were not altered by prior occlusion of the efferent arteriole, suggesting that afferent vasoconstriction does not represent a myogenic reaction to an increase in efferent resistance. The vasoconstrictor response to ANG II was largely eliminated by removal of the glomerulus and the distal-most portion of the afferent arteriole, whereas the response to vasopressin remained intact. Our data are consistent with the notion that the juxtaglomerular apparatus (JGA) and/or glomerulus may control proximal afferent arteriolar contractility by electrotonic or myogenic coupling mechanisms or by producing cofactors that modulate vasomotor responses.
35
Koller, A., E. J. Messina, M. S. Wolin, and G. Kaley. "Effects of endothelial impairment on arteriolar dilator responses in vivo." American Journal of Physiology-Heart and Circulatory Physiology 257, no. 5 (November 1, 1989): H1485—H1489. http://dx.doi.org/10.1152/ajpheart.1989.257.5.h1485.
Full textAbstract:
In pentobarbital-anesthetized rats we investigated the role of the endothelium in the dilation of third-order arterioles of cremaster muscle to acetylcholine, adenosine, and sodium nitroprusside in vivo. Responses to the topical administration of these agents were measured with image shearing and recorded with video microscopy before and after light-dye (L-D) treatment of a 50- to 100-microns segment of the arteriole under study. L-D treatment consisted of intravascular administration of sodium fluorescein and the illumination of a discrete area of the arteriole under study with its excitation light from a mercury lamp. Before L-D treatment, acetylcholine (10(-7) to 10(-5) M) and adenosine (10(-6) to 10(-4) M) produced dose-dependent increases in arteriolar diameter (vasodilation). After L-D treatment of the arteriolar segment, administration of 10(-7) M acetylcholine evoked a vasoconstriction (-19% from control), and the dilator responses to 10(-6) and 10(-5) M were inhibited by 91 and 77%, respectively. In contrast, the arteriolar dilator responses to all doses of adenosine and sodium nitroprusside (2 x 10(-7) M) were not altered by this treatment. In addition, the dilator responses to acetylcholine were not changed in the nonilluminated, distal, and proximal segments of the arterioles. These findings suggest that L-D treatment selectively alters the function of the endothelium resulting in the loss of vasodilation to acetylcholine, whereas arteriolar smooth muscle function does not appear to be affected.
36
Bock, H. A., M. Hermle, A. Fiallo, R. W. Osgood, and T. A. Fried. "Measurement of renin secretion in single perfused rabbit glomeruli." American Journal of Physiology-Renal Physiology 258, no. 5 (May 1, 1990): F1460—F1465. http://dx.doi.org/10.1152/ajprenal.1990.258.5.f1460.
Full textAbstract:
A new technique is presented that allows the measurement of the renin secretion rate of single rabbit glomeruli during in vitro perfusion at controlled afferent arteriolar perfusion pressure. Rabbit glomeruli with intact afferent arteriole and Bowman's capsule are obtained by microdissection and cannulated with a pipette system that allows continuous afferent arteriolar pressure measurement. The renin secretion rate of 10 glomeruli, perfused at 40 mmHg, was measured in 15-min intervals with an antibody-trapping microassay. Renin secretion rate was low relative to total renin content (1.2-2.0% of content/perfusion h) and increased three- to fivefold in response to isoproterenol (10(-5) M). The afferent arteriole contracted to norepinephrine (10(-5) M) in each instance. This novel, although difficult, technique allows the study of renin release in vitro at controlled perfusion pressure, without the interfering effects of the macula densa, arterial angiotensin II, and the adrenergic nervous system. It should allow a new perspective on issues such as the pressure-flow dependence of renin release and the interaction of the afferent arteriolar endothelium with the renin-secreting juxtaglomerular cells.
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Shih, Andy Y., Beth Friedman, Patrick K. Drew, Philbert S. Tsai, Patrick D. Lyden, and David Kleinfeld. "Active Dilation of Penetrating Arterioles Restores Red Blood Cell Flux to Penumbral Neocortex after Focal Stroke." Journal of Cerebral Blood Flow & Metabolism 29, no. 4 (January 28, 2009): 738–51. http://dx.doi.org/10.1038/jcbfm.2008.166.
Full textAbstract:
Pial arterioles actively change diameter to regulate blood flow to the cortex. However, it is unclear whether arteriole reactivity and its homeostatic role of conserving red blood cell (RBC) flux remains intact after a transient period of ischemia. To examine this issue, we measured vasodynamics in pial arteriole networks that overlie the stroke penumbra during transient middle cerebral artery occlusion in rat. In vivo two-photon laser-scanning microscopy was used to obtain direct and repeated measurements of RBC velocity and lumen diameter of individual arterioles, from which the flux of RBCs was calculated. We observed that occlusion altered surface arteriole flow patterns in a manner that ensured undisrupted flow to penetrating arterioles throughout the imaging field. Small-diameter arterioles (< 23 µm), which included 88% of all penetrating arterioles, exhibited robust vasodilation over a 90-min occlusion period. Critically, persistent vasodilation compensated for an incomplete recovery of RBC velocity during reperfusion to enable a complete restoration of postischemic RBC flux. Further, histologic examination of tissue hypoxia suggested re-oxygenation through all cortical layers of the penumbra. These findings indicate that selective reactivity of small pial arterioles is preserved in the stroke penumbra and acts to conserve RBC flux during reperfusion.
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Vis, M. A., P. Sipkema, and N. Westerhof. "Compression of intramyocardial arterioles during cardiac contraction is attenuated by accompanying venules." American Journal of Physiology-Heart and Circulatory Physiology 273, no. 2 (August 1, 1997): H1003—H1011. http://dx.doi.org/10.1152/ajpheart.1997.273.2.h1003.
Full textAbstract:
It was calculated how cardiac contraction influences the luminal cross-sectional area of a maximally dilated coronary arteriole (37-micron inner diameter at a pressure of 35 mmHg) that is accompanied by two equal venules (45-micron inner diameter at a pressure of 17 mmHg), forming a so-called "triad." It was found that, during a contraction with 14% cardiac muscle shortening, arteriolar area is virtually unaffected (increase of 4%) at the expense of a large (55%) decrease in venular area. For comparison, the areas of an unaccompanied arteriole and an unaccompanied venule were calculated to be reduced by 45 and 36%, respectively, demonstrating the "protective effect" on accompanied arterioles in a triad. During contraction, the overall resistance of a system consisting of one arteriole in series with two parallel venules of equal length was calculated to increase about twice as much for nonaccompanied vessels (resistance increases by a factor of 2.8) than for vessels in a triad arrangement (resistance increased by a factor of 1.4). The calculations show that the extravascular (intramyocardial) pressure, which determines vascular area, is not an independent variable as in the intramyocardial pump and waterfall models but depends on the vascular "loading" conditions. Thus the small venular pressure together with the large venular compliance causes the extravascular pressure to remain low during contraction, thereby protecting the stiff arteriole at high pressure. We conclude that the triad arrangement of intramyocardial coronary vessels attenuates the increase in coronary resistance during cardiac contraction and thus has an important functional advantage.
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Rivers, R. J. "Cumulative conducted vasodilation within a single arteriole and the maximum conducted response." American Journal of Physiology-Heart and Circulatory Physiology 273, no. 1 (July 1, 1997): H310—H316. http://dx.doi.org/10.1152/ajpheart.1997.273.1.h310.
Full textAbstract:
The vascular network functions to distribute blood flow to the tissues that require it, and conducted vasodilation may facilitate this function. Experiments on arterioles in anesthetized hamster cheek pouch modeled the conducted responses that may come from a series of neighboring capillary modules and determined whether cumulative conducted responses could thereby maximally dilate upstream arterioles. Methacholine (10(-5) M) was simultaneously microapplied on an arteriole (resting diameter, approximately 22 microns; maximum diameter, approximately 47 microns) from one to four micropipettes spaced 100 microns apart, and with each added pipette the conducted dilation increased (up to a maximum dilation of approximately 5 microns). Increasing the methacholine 10-fold (10(-4) M) did not further increase the conducted response. The conducted response could also not be increased by lengthening the duration of microapplication. Yet, dilations that were not cumulative along a single arteriole became cumulative when initiated instead on adjacent arterioles. Therefore, these data demonstrate that conducted dilation along a single arteriole is limited and, if this model is correct, suggest that neighboring capillary modules may communicate only a limited conducted response to the network.
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Beard, Daniel J., Damian D. McLeod, Caitlin L. Logan, Lucy A. Murtha, Mohammad S. Imtiaz, Dirk F. van Helden, and Neil J. Spratt. "Intracranial Pressure Elevation Reduces Flow through Collateral Vessels and the Penetrating Arterioles they Supply. a Possible Explanation for ‘Collateral Failure’ and Infarct Expansion after Ischemic Stroke." Journal of Cerebral Blood Flow & Metabolism 35, no. 5 (February 11, 2015): 861–72. http://dx.doi.org/10.1038/jcbfm.2015.2.
Full textAbstract:
Recent human imaging studies indicate that reduced blood flow through pial collateral vessels (‘collateral failure’) is associated with late infarct expansion despite stable arterial occlusion. The cause for ‘collateral failure’ is unknown. We recently showed that intracranial pressure (ICP) rises dramatically but transiently 24 hours after even minor experimental stroke. We hypothesized that ICP elevation would reduce collateral blood flow. First, we investigated the regulation of flow through collateral vessels and the penetrating arterioles arising from them during stroke reperfusion. Wistar rats were subjected to intraluminal middle cerebral artery (MCA) occlusion (MCAo). Individual pial collateral and associated penetrating arteriole blood flow was quantified using fluorescent microspheres. Baseline bidirectional flow changed to MCA-directed flow and increased by 4450% immediately after MCAo. Collateral diameter changed minimally. Second, we determined the effect of ICP elevation on collateral and watershed penetrating arteriole flow. Intracranial pressure was artificially raised in stepwise increments during MCAo. The ICP increase was strongly correlated with collateral and penetrating arteriole flow reductions. Changes in collateral flow post-stroke appear to be primarily driven by the pressure drop across the collateral vessel, not vessel diameter. The ICP elevation reduces cerebral perfusion pressure and collateral flow, and is the possible explanation for ‘collateral failure’ in stroke-in-progression.
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Koller, A., and G. Kaley. "Role of endothelium in reactive dilation of skeletal muscle arterioles." American Journal of Physiology-Heart and Circulatory Physiology 259, no. 5 (November 1, 1990): H1313—H1316. http://dx.doi.org/10.1152/ajpheart.1990.259.5.h1313.
Full textAbstract:
In cremaster muscle of pentobarbital-anesthetized rats, the role of endothelium in the reactive dilation of an arteriole (mean control diameter: 18.2 +/- 0.5 microns) during and after short (approximately 20 s) or long (approximately 80 s) occlusion of a parent arteriole was investigated. Distal to the occluder, arteriolar diameter increased during the occlusion (mean peak increase: 6.9 +/- 0.4 and 6.7 +/- 1.1 microns, respectively) and increased even further after the release of the occlusion as blood flow was reestablished (additional mean increase: 6.5 +/- 0.7 and 5.8 +/- 0.8 microns, respectively). The duration of arteriolar dilation after the release of the occlusion was dependent on the duration of occlusion (252.2 +/- 37 vs. 411.3 +/- 57 s; P less than 0.05). After impairment of the arteriolar endothelium by light/dye treatment, a dilation was still present during both the shorter and longer occlusions (mean increase: 4.73 +/- 1.4 and 4.73 +/- 1.3 microns, respectively); however, in both cases the additional dilation after release of the occlusion was greatly diminished. The duration of reactive arteriolar responses following impairment of the endothelium was significantly reduced only on release of the shorter occlusions. The results suggest that reactive dilation (hyperemia) of arterioles is the result of multiple, endothelium-dependent and endothelium-independent vasoactive factors.
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Weihprecht, H., J. N. Lorenz, J. P. Briggs, and J. Schnermann. "Vasomotor effects of purinergic agonists in isolated rabbit afferent arterioles." American Journal of Physiology-Renal Physiology 263, no. 6 (December 1, 1992): F1026—F1033. http://dx.doi.org/10.1152/ajprenal.1992.263.6.f1026.
Full textAbstract:
To examine the vasomotor effects of purinergic agonists, experiments were performed in isolated afferent arterioles of rabbit kidneys dissected together with their glomerulus and perfused with a pressure head of 120 cmH2O. Changes in vascular diameter were taken as measure of changes in vasomotor tone. Adenosine caused a dose-dependent and persistent decrease in vascular diameter along the entire afferent arteriole with significant changes being detectable at 10(-8) M. Constrictor effects were more pronounced in the glomerular entrance segment of the arteriole where adenosine caused a progressive diameter reduction with maximum contraction at 10(-4) M. Similar monophasic diameter reductions of the distal afferent arteriole were seen with increasing bath concentrations of 2-chloroadenosine (2-ClAdo), cyclohexyladenosine (CHA), and 5'-(N-ethylcarboxamido)adenosine (NECA). Concentrations to achieve half-maximum responses were 92.5 nM for 2-ClAdo, 39 nM for CHA, and 107 nM for NECA. The A2-receptor agonist N6-[2-(3,5-dimethoxyphenyl)-2-(2-methylphenyl)ethyl]adenosine had no effect on vessel diameter. Increasing bath concentrations of ATP caused significant diameter reductions in both the proximal and distal parts of the afferent arterioles. Addition of the A1-receptor blocker, 8-cyclopentyl-1,3-dipropylxanthine, eliminated the effect of ATP in the proximal region of the arteriole, but a significant diameter reduction was still seen in the glomerular entrance segment. The ATP analogue, beta gamma-methylene-ATP, caused a significant diameter reduction in this segment. These results are consistent with an essentially exclusive presence of A1 receptors in the glomerular entrance segment of the afferent arteriole, whereas in more proximal regions A2 receptors appear to also be expressed in low density. These studies also provide functional evidence for the presence of P2x receptors in renal afferent arterioles.
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Yan, Shuangquan, Yiran Wang, Panpan Liu, Ali Chen, Mayun Chen, Dan Yao, Xiaomei Xu, Liangxing Wang, and Xiaoying Huang. "Baicalin Attenuates Hypoxia-Induced Pulmonary Arterial Hypertension to Improve Hypoxic Cor Pulmonale by Reducing the Activity of the p38 MAPK Signaling Pathway and MMP-9." Evidence-Based Complementary and Alternative Medicine 2016 (2016): 1–9. http://dx.doi.org/10.1155/2016/2546402.
Full textAbstract:
Baicalin has a protective effect on hypoxia-induced pulmonary hypertension in rats, but the mechanism of this effect remains unclear. Thus, investigating the potential mechanism of this effect was the aim of the present study. Model rats that display hypoxic pulmonary hypertension and cor pulmonale under control conditions were successfully generated. We measured a series of indicators to observe the levels of pulmonary arterial hypertension, pulmonary arteriole remodeling, and right ventricular remodeling. We assessed the activation of p38 mitogen-activated protein kinase (MAPK) in the pulmonary arteriole walls and pulmonary tissue homogenates using immunohistochemistry and western blot analyses, respectively. The matrix metalloproteinase- (MMP-) 9 protein and mRNA levels in the pulmonary arteriole walls were measured using immunohistochemistry and in situ hybridization. Our results demonstrated that baicalin not only reduced p38 MAPK activation in both the pulmonary arteriole walls and tissue homogenates but also downregulated the protein and mRNA expression levels of MMP-9 in the pulmonary arteriole walls. This downregulation was accompanied by the attenuation of pulmonary hypertension, arteriole remodeling, and right ventricular remodeling. These results suggest that baicalin may attenuate pulmonary hypertension and cor pulmonale, which are induced by chronic hypoxia, by downregulating the p38 MAPK/MMP-9 pathway.
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Dora, Kim A., Jun Xia, and Brian R. Duling. "Endothelial cell signaling during conducted vasomotor responses." American Journal of Physiology-Heart and Circulatory Physiology 285, no. 1 (July 2003): H119—H126. http://dx.doi.org/10.1152/ajpheart.00643.2002.
Full textAbstract:
ACh and KCl stimulate vasomotor responses that spread rapidly and bidirectionally along arteriole walls, most likely via spread of electric current or Ca2+ through gap junctions. We examined these possibilities with isolated, cannulated, and perfused hamster cheek pouch arterioles (50- to 80-μm resting diameter). After intraluminal loading of 2 μM fluo 3 to measure Ca2+ or 1 μM di-8-ANEPPS to measure membrane potential, photometric techniques were used to selectively measure changes in intracellular Ca2+ concentration ([Ca2+]i) or membrane potential in endothelial cells. Activation of the endothelium by micropipette application of ACh (10-4 M, 1.0-s pulse) to a short segment of arteriole (100–200 μm) increased endothelial cell [Ca2+]i and caused hyperpolarization at the site of stimulation. This response was followed rapidly by vasodilation of the entire arteriole (∼2-mm length). Change in membrane potential always preceded dilation, both at the site of stimulation and at distant sites along the arteriole. In contrast, an increase in endothelial cell [Ca2+]i was observed only at the application site. Micropipette application of KCl, which can depolarize both smooth muscle and endothelial cells (250 mM, 2.5-s pulse), also caused a rapid, spreading response consisting of depolarization followed by vasoconstriction. With KCl stimulation, in addition to changes in membrane potential, increases in endothelial cell [Ca2+]i were observed at distant sites not directly exposed to KCl. The rapid longitudinal spread of both hyperpolarizing and depolarizing responses support electrical coupling as the mode of signal transmission along the arteriolar length. In addition, the relatively short distance between heterologous cell types enables the superimposed radial Ca2+ signaling between smooth muscle and endothelial cells to modulate vasomotor responses.
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Trottier, Greg, Morley Hollenberg, Xuemei Wang, Yu Gui, Kathy Loutzenhiser, and Rodger Loutzenhiser. "PAR-2 elicits afferent arteriolar vasodilation by NO-dependent and NO-independent actions." American Journal of Physiology-Renal Physiology 282, no. 5 (May 1, 2002): F891—F897. http://dx.doi.org/10.1152/ajprenal.00233.2001.
Full textAbstract:
Proteinase-activated receptors (PARs) are a novel class of G protein-coupled receptors that respond to signals through endogenous proteinases. PAR activation involves enzymatic cleavage of the extracellular NH2-terminal domain and unmasking of a new NH2 terminus, which serves as an anchored ligand to activate the receptor. At least four PAR subtypes have been identified. In the present study, we used the in vitro perfused hydronephrotic rat kidney to examine the effects of activating PAR-2 on the afferent arteriole. The synthetic peptide SLIGRL-NH2, which corresponds to the exposed ligand sequence and selectively activates PAR-2, did not alter basal afferent arteriolar diameter but caused a concentration-dependent vasodilation (3–30 μM) of arterioles preconstricted by angiotensin II (0.1 nM). A modified peptide sequence (LSIGRL-NH2, inactive at PAR-2) had no effect. This vasodilation was characterized by an initial transient component followed by a smaller sustained response. A similar pattern of vasodilation was seen when SLIGRL-NH2 was administered to isolated perfused normal rat kidney. The sustained component of the PAR-2-induced afferent arteriolar vasodilation was eliminated by nitric oxide (NO) synthase inhibition (100 μM nitro-l-arginine methyl ester). In contrast, the transient vasodilation persisted under these conditions. This transient response was not observed when afferent arterioles were preconstricted with elevated KCl, suggesting involvement of an endothelium-derived hyperpolarizing factor. Finally, RT-PCR revealed the presence of PAR-2 mRNA in isolated afferent arterioles. These findings indicate that PAR-2 is expressed in the afferent arteriole and that its activation elicits afferent arteriolar vasodilation by NO-dependent and NO-independent mechanisms.
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Neyman, Michael, Jamie Gewitz, and Mortimer Poncz. "Platelet-Delivered Factor VIII (FVIII) Decreases Thrombus Stability." Blood 108, no. 11 (November 16, 2006): 1602. http://dx.doi.org/10.1182/blood.v108.11.1602.1602.
Full textAbstract:
Abstract FVIII is normally not expressed by developing megakaryocytes. We have previously developed a transgenic mice in whom human B-domainless FVIII (hbdFVIII) was expressed specifically within developing megakaryocytes and stored in α-granules. This platelet (p) FVIII was especially potent in correcting bleeding in a FeCl3 carotid artery injury model. In FVIIInull mice, ~5% pFVIII plasma equivalency was as effective as a >25% plasma correction in normalizing thrombosis in this model. One concern with our observation was whether this enhanced efficacy would lead to an arterial prothrombotic state. We, therefore studied the details of pFVIII-dependent thrombosis using the cremaster arteriole/venule laser injury model, simultaneously monitoring platelet accumulation and fibrin clot growth at the site of injury (>30 injuries per study). Baseline studies in FVIIInull mice show that these mice had a decrease in platelet plug growth to ~50% of WT mice after either arteriole or venule injury. Fibrin accumulation was decreased after arteriole injury to ~20% of WT and was barely detectable after venule injury at ~3% of WT. Time to onset of fibrin clot formation on the arteriole side was delayed from the normal 30 sec to >50 secs and on the venule side from the normal of 40 secs to >60 secs. Stepwise improvement in platelet plug size, and size and time to onset of fibrin clot was seen with increasing amounts of hbdFVIII infusions. pFVIII/FVIIInull mice had decreased platelet plug formation compared to WT mice on both the arterial side (~10% of WT) and venule side (~25%). Fibrin accumulation was similar to the FVIIInull animals after arterial injury, but time to onset of clot was normalized. On the venule side, fibrin accumulation was 2–3 times that of the FVIIInull mice and again time to onset was normalized. Individual films of the pFVIII/FVIIInull suggested that these animals showed more clot instability than WT mice or FVIIInull mice. Indeed, quantitative analysis of downstream embolization showed that the pFVIII/FVIIInull mice had a significant increase in detectable emboli per 3 min study compared to WT mice (7.3 vs. 5.0 arterial and 6.3 vs. 0.5 venule, ns arterial and p<0.05 venule), but not compared to FVIIInull mice with or without a 25% hbdFVIII correction. Importantly, the size of the average emboli (in relative light units) in the pFVIII/FVIIInull mice was increased 10-fold (112 ± 224 arteriole and 145 ± 339 venule) vs. WT (11.6 ± 12.9 arteriole and 14.5 ± 13.1 venule, each p <0.0001) and vs. FVIIInull mice after a 25% correction (9.6 ± 15.6 arteriole and 24.2 ± 30.9 venule, each p<0.001). Compared to the FVIIInull mice, the average embolus was significantly (p<0.001) larger only on the venule side (74.1 ± 108 arteriole and 18.8 ± 12.2 venule). Thus, FVIIInull mice have a clear defect in cremaster laser injury studies affecting venule more than arterial fibrin formation with a concomitant defects in platelet plug formation. pFVIII improves venule more than arteriole fibrin clot formation but only to a level equivalent to the pFVIII content. There was no improvement in platelet plug formation, but there was enhanced thrombus embolization. These data suggest that pFVIII alters the details of thrombus structure with associated decrease in clot stability, especially on the venous side, suggesting that platelet-delivered FVIII may be associated with an increased risk of embolization.
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Edwards, RM. "Direct Assessment of Glomerular Arteriole Reactivity." Physiology 3, no. 5 (October 1, 1988): 216–19. http://dx.doi.org/10.1152/physiologyonline.1988.3.5.216.
Full textAbstract:
The glomerular arterioles play an important role in the regulation of renal blood flow and glomerular filtration rate. The need to understand how glomerular arteriole resistance is regulated has led to the development of new techniques to directly study these important segments of the renal microvasculature in vitro and in situ.
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Jackson, W. F. "Arteriolar oxygen reactivity: where is the sensor?" American Journal of Physiology-Heart and Circulatory Physiology 253, no. 5 (November 1, 1987): H1120—H1126. http://dx.doi.org/10.1152/ajpheart.1987.253.5.h1120.
Full textAbstract:
The hypothesis that arterioles are intrinsically sensitive to oxygen was tested by comparing arteriolar diameter responses with local and global PO2 changes in superfused hamster cheek pouch preparations. Local PO2 changes were produced by microapplication of fluid onto the surface of occluded or unoccluded aparenchymal arterioles or by cannulation and perfusion of arterioles in situ. Global changes refer to PO2 changes in the superfusate flowing over the entire preparation. Local, effective PO2 changes had no significant effect on arteriolar diameters. In contrast, global PO2 changes produced significant, reproducible changes in diameter. These observations do not support the hypothesis that arterioles are intrinsically oxygen sensitive, unless the oxygen-sensitive sites are distributed sparsely along the arteriolar tree. The data are consistent with oxygen sensors located either in vessels downstream from 15-micron arterioles (in terminal arterioles, capillaries, or venules) or in the parenchyma. The data also suggest that these sensors detect changes in PO2 and then initiate responses that can be conducted along the vasculature to an arteriole distant from the sensor.
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Cryer, H. G., R. N. Garrison, P. D. Harris, B. H. Greenwald, and N. L. Alsip. "Prostaglandins mediate skeletal muscle arteriole dilation in hyperdynamic bacteremia." American Journal of Physiology-Heart and Circulatory Physiology 259, no. 3 (September 1, 1990): H728—H734. http://dx.doi.org/10.1152/ajpheart.1990.259.3.h728.
Full textAbstract:
Live Escherichia coli bacteremia during the high cardiac output (hyperdynamic) phase of sepsis causes constriction of large arterioles but dilation of small arterioles in skeletal muscle. This study examines the role of dilator prostaglandins, serotonin, and histamine in these differential microvascular responses in the decerebrate rat that avoids the effects of drug anesthesia. Topical application of meclofenamate, a prostaglandin synthesis inhibitor, to the cremaster muscle 60 min after induction of E. coli bacteremia enhanced the constriction of large arterioles from 20 +/- 8 to 46 +/- 9% less than baseline and blunted the dilation of small arterioles from 39 +/- 9 to 17 +/- 7% above baseline values in the cremaster microcirculation. Induction of E. coli bacteremia after pretreatment of the cremaster with meclofenamate constricted large arterioles to 40 +/- 4% less than baseline and small arterioles to 31 +/- 4% less than baseline. This indicates that prostaglandins initiate small arteriole dilation in response to E. coli, but some other dilator factor is activated by prostaglandins to maintain small arteriole dilation during E. coli bacteremia. Topical application of cyproheptadine, an antagonist of both histamine and serotonin receptors, to the cremaster muscle did not alter the E. coli-induced constriction of large arterioles or the dilation of small arterioles in the cremaster microcirculation.
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Tyml, Karel, Jingcheng Yu, and David G. McCormack. "Capillary and arteriolar responses to local vasodilators are impaired in a rat model of sepsis." Journal of Applied Physiology 84, no. 3 (March 1, 1998): 837–44. http://dx.doi.org/10.1152/jappl.1998.84.3.837.
Full textAbstract:
Although sepsis is known to affect vascular function, little is known about changes at the capillary level. We hypothesized that sepsis attenuates the “upstream” arteriolar response to vasoactive agents applied locally to capillaries. Sepsis in rats was induced by cecal ligation and perforation. After 24 h, extensor digitorum longus muscle was prepared for intravital microscopy. Phenylephrine (PE, 10 mM) and acetylcholine (ACh, 10 mM) were applied iontophoretically on terminal arterioles and on their downstream daughter capillaries (300 μm from arteriole). There was no significant difference between control and septic rats in baseline arteriolar diameters [8.0 ± 0.6 vs. 9.8 ± 0.8 (SE) μm] or baseline red blood cell velocity ( V RBC) in perfused daughter capillaries (255 ± 10 vs. 264 ± 13 μm/s). Application of PE onto arterioles resulted in comparable constrictions (i.e., −22% diameter change) and V RBC reductions (−100%) in control and septic rats. In contrast, arteriolar diameter and V RBCincreases after application of ACh were attenuated in sepsis (diameter: from 41 to 14%; V RBC: from 67 to 24%). Application of PE onto the capillary reduced V RBC to the same level (−100%) in both groups, whereas application of ACh increased V RBCless in septic than in control rats (20 vs. 73%). On the basis of arteriolar-capillary pair stimulations, sepsis affected V RBC responses to ACh more in the capillary than in the arteriole. When the adenosine analog 5′- N-ethylcarboxamidoadenosine (0.1 mM) was used instead of ACh, similar effects of sepsis were seen. To test for a possible involvement of inducible NO synthase (iNOS) in sepsis-induced attenuated ACh responses, arterioles and capillaries in septic animals were locally pretreated with the iNOS blocker aminoguanidine (10 mM). In both microvessels, aminoguanidine restored the ACh response to the control level. We conclude that impaired capillary V RBCand arteriolar diameter responses to vasodilators applied to capillaries in septic rat skeletal muscle were due to dysfunction at arteriolar and capillary levels. The study underscores the significant role iNOS/NO may play in sepsis-induced alteration of vascular reactivity in vivo.