Academic literature on the topic 'Arteriolar myogenic tone'
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Journal articles on the topic "Arteriolar myogenic tone"
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Davis, Michael J., and Judy Davidson. "Force-velocity relationship of myogenically active arterioles." American Journal of Physiology-Heart and Circulatory Physiology 282, no. 1 (January 1, 2002): H165—H174. http://dx.doi.org/10.1152/ajpheart.2002.282.1.h165.
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We compared the shortening velocity of smooth muscle in arterioles that had low or high levels of myogenic tone or norepinephrine (NE)-induced tone. We hypothesized that enhanced myogenic tone of arterioles reflects an enhanced maximum velocity of shortening of arteriolar smooth muscle in a way that is different from that produced by NE. These concepts are untested assumptions of arteriolar mechanics. Second-order arterioles from hamster cheek pouch (passive diameter at 40 mmHg = 42 μm) were isolated and cannulated for in vitro study. In the absence of flow, pressure was controlled by hydraulic pumps so that servo control of wall tension could be achieved from measurement of internal diameter and pressure. Isotonic quick-release protocols were used to measure the initial velocity of shortening following release from control wall tension (afterload) to a series of fractional afterloads. After release, the initial rates of shortening were fit to the Hill equation to obtain coefficients for a hyperbolic fit of the velocity-afterload relationship. The maximal unloaded shortening velocity for partially activated arterioles ( V′max) was determined from the y-intercept of each plot. Using this procedure, we compared V′max from two groups of arterioles equilibrated at low or high pressure, i.e., with low or high myogenic tone. Arterioles with higher myogenic tone had higher values of V′max than arterioles with lower myogenic tone. V′max for arterioles partially activated with NE at low pressure was comparable to V′max for arterioles with high myogenic tone, but NE produced high velocities at low force, whereas enhanced myogenic tone produced roughly parallel shifts in velocity and force. The results suggest that increased myogenic tone does indeed reflect enhanced activation of arteriolar smooth muscle, and this effect is mechanically different from that produced by NE.
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Spurrell, Brian E., Timothy V. Murphy, and Michael A. Hill. "Tyrosine phosphorylation modulates arteriolar tone but is not fundamental to myogenic response." American Journal of Physiology-Heart and Circulatory Physiology 278, no. 2 (February 1, 2000): H373—H382. http://dx.doi.org/10.1152/ajpheart.2000.278.2.h373.
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The present study investigated the role of protein tyrosine phosphorylation in myogenic responsiveness of rat skeletal muscle arterioles. Arteriolar segments were cannulated and pressurized without intraluminal flow. All vessels studied developed spontaneous tone and demonstrated significant myogenic constriction to step changes in pressure with a resultant increase in myogenic tone over an intraluminal pressure range of 50–150 mmHg. Step increases in intraluminal pressure from 50 to 120 mmHg caused a rapid and sustained elevation in intracellular [Ca2+], as measured using fura 2. Vessels with myogenic tone dilated in response to tyrosine kinase inhibitors genistein (10 or 30 μM) and tyrphostin A47 (10 or 30 μM) and constricted to the tyrosine phosphatase inhibitor pervanadate (1 or 10 μM). Despite the dilator effect, myogenic reactivity was not blocked by the inhibitors. Daidzein (10 μM), a compound structurally similar to genistein but without tyrosine kinase-inhibiting activity, did not alter vessel tone or myogenic responses. Preincubation of arterioles with genistein or tyrphostin A47 did not significantly alter baseline arteriolar [Ca2+], and neither drug reduced the increase in [Ca2+] following an acute increase in intraluminal pressure. Constriction induced by pervanadate (10 μM) was not accompanied by a significant increase in intracellular [Ca2+], even though removal of extracellular Ca2+ reversed the constriction. Examination of smooth muscle tyrosine phosphorylation, using a fluorescent phosphotyrosine antibody and confocal microscopy, showed that increased intraluminal pressure resulted in an increase in anti-phosphotyrosine fluorescence. Because manipulation of tyrosine kinase activity was found to alter vessel diameter, these data support a role for tyrosine phosphorylation in modulation of arteriolar tone. However, the results indicate that acute arteriolar myogenic constriction does not require tyrosine phosphorylation.
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Heaps, Cristine L., and Douglas K. Bowles. "Nonuniform changes in arteriolar myogenic tone within skeletal muscle following hindlimb unweighting." Journal of Applied Physiology 92, no. 3 (March 1, 2002): 1145–51. http://dx.doi.org/10.1152/japplphysiol.01031.2000.
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Hindlimb unweighting (HLU) has been shown to alter myogenic tone distinctly in arterioles isolated from skeletal muscles composed predominantly of fast-twitch (white gastrocnemius) compared with slow-twitch (soleus) fibers. Based on these findings, we hypothesized that HLU would alter myogenic tone differently in arterioles isolated from distinct fiber-type regions within a single skeletal muscle. We further hypothesized that alterations in myogenic tone would be associated with alterations in voltage-gated Ca2+ channel current (VGCC) density of arteriolar smooth muscle. After 14 days of HLU or weight bearing (control), first-order arterioles were isolated from both fast-twitch and mixed fiber-type regions of the gastrocnemius muscle, cannulated, and pressurized at 90 cmH2O. Mixed gastrocnemius arterioles of HLU rats demonstrated increased spontaneous tone [43 ± 5% (HLU) vs. 27 ± 4% (control) of possible constriction] and an approximately twofold enhanced myogenic response when exposed to step changes in intraluminal pressure (10–130 cmH2O) compared with control rats. In contrast, fast-twitch gastrocnemius arterioles of HLU rats demonstrated similar levels of spontaneous tone [6 ± 2% (HLU) vs. 6 ± 2% (control)] and myogenic reactivity to control rats. Neither KCl-induced contractile responses (10–50 mM KCl) nor VGCC density was significantly different between mixed gastrocnemius arterioles of HLU and control rats. These results suggest that HLU produces diverse adaptations in myogenic reactivity of arterioles isolated from different fiber-type regions of a single skeletal muscle. Furthermore, alterations in myogenic responses were not attributable to altered VGCC density.
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Davis, M. J. "Myogenic response gradient in an arteriolar network." American Journal of Physiology-Heart and Circulatory Physiology 264, no. 6 (June 1, 1993): H2168—H2179. http://dx.doi.org/10.1152/ajpheart.1993.264.6.h2168.
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Experiments were conducted to test the hypothesis that a longitudinal gradient in myogenic responsiveness exists within an arteriolar network. Single arterioles were dissected from the hamster cheek pouch, cannulated with micropipettes, and transferred to an inverted microscope for in vitro study. Pressure-diameter relationships of five branching orders of arterial vessels were measured in the presence of spontaneous vascular tone and after elimination of tone with a Ca(2+)-free solution containing nitroprusside. At luminal pressures matching those found in vivo, the diameters of the vessels with spontaneous tone were as follows: small arteries, 81 microns; first-order arterioles, 52 microns; second-order arterioles, 32 microns; third-order arterioles, 24 microns; and fourth-order arterioles, 11 microns. All branching orders of vessels exhibited true myogenic responses as indicated by negative slopes of their pressure-diameter relationships. Each vascular branching order exhibited its maximum myogenic responsiveness at a pressure near or just slightly higher than its normal pressure as measured in vivo. Relative myogenic responsiveness increased with decreasing vessel size down to the level of the second- and third-order arterioles, whereas fourth-order arterioles were substantially less responsive than third-order arterioles. A compilation of data from numerous in vivo and in vitro studies suggests that the same myogenic response pattern may be found in other vascular beds.
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Ungvari, Zoltan, and Akos Koller. "Selected Contribution: NO released to flow reduces myogenic tone of skeletal muscle arterioles by decreasing smooth muscle Ca2+sensitivity." Journal of Applied Physiology 91, no. 1 (July 1, 2001): 522–27. http://dx.doi.org/10.1152/jappl.2001.91.1.522.
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To clarify the contribution of intracellular Ca2+ concentration ([Ca2+]i)-dependent and -independent signaling mechanisms in arteriolar smooth muscle (aSM) to modulation of arteriolar myogenic tone by nitric oxide (NO), released in response to increases in intraluminal flow from the endothelium, changes in aSM [Ca2+]i and diameter of isolated rat gracilis muscle arterioles (pretreated with indomethacin) were studied by fluorescent videomicroscopy. At an intraluminal pressure of 80 mmHg, [Ca2+]i significantly increased and myogenic tone developed in response to elevations of extracellular Ca2+ concentration. The Ca2+ channel inhibitor nimodipine substantially decreased [Ca2+]i and completely inhibited myogenic tone. Dilations to intraluminal flow (that were inhibited by N ω-nitro-l-arginine methyl ester) or dilations to the NO donor S-nitroso- N-acetyl-dl-penicillamine (that were inhibited by the guanylate cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one) were not accompanied by substantial decreases in aSM [Ca2+]i. 8-Bromoguanosine cGMP and the cGMP-specific phosphodiesterase inhibitor zaprinast significantly dilated arterioles yet elicited only minimal decreases in [Ca2+]i. Thus flow-induced endothelial release of NO elicits relaxation of arteriolar smooth muscle by a cGMP-dependent decrease of the Ca2+ sensitivity of the contractile apparatus without substantial changes in the pressure-induced level of [Ca2+]i.
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Brayden, Joseph E., Yao Li, and Matthew J. Tavares. "Purinergic Receptors Regulate Myogenic Tone in Cerebral Parenchymal Arterioles." Journal of Cerebral Blood Flow & Metabolism 33, no. 2 (November 21, 2012): 293–99. http://dx.doi.org/10.1038/jcbfm.2012.169.
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Myogenic tone is a fundamental aspect of vascular behavior in resistance arteries. This contractile response to changes in intravascular pressure is critically involved in blood flow autoregulation in tissues such as the brain, kidneys, and heart. Myogenic tone also helps regulate precapillary pressure and provides a level of background tone upon which vasodilator stimuli act to increase tissue perfusion when appropriate. Despite the importance of these processes in the brain, little is known about the mechanisms involved in control of myogenic tone in the cerebral microcirculation. Here, we report that pharmacological inhibition of P2Y4 and P2Y6 pyrimidine receptors nearly abolished myogenic tone in cerebral parenchymal arterioles (PAs). Molecular suppression of either P2Y4 or P2Y6 receptors using antisense oligodeoxynucleotides reduced myogenic tone by 44% ± 8% and 45% ± 7%, respectively. These results indicate that both receptor isoforms are activated by increased intravascular pressure, which enhances the activity of voltage-dependent calcium channels and increases myogenic tone in PAs. Enhancement or inhibition of ectonucleotidase activity had no effect on parenchymal arteriolar myogenic tone, indicating that this response is not mediated by local release of nucleotides, but rather may involve direct mechanical activation of P2Y receptors in the smooth muscle cells.
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Hill, Michael A., Gerald A. Meininger, Michael J. Davis, and Ismail Laher. "Therapeutic potential of pharmacologically targeting arteriolar myogenic tone." Trends in Pharmacological Sciences 30, no. 7 (July 2009): 363–74. http://dx.doi.org/10.1016/j.tips.2009.04.008.
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Jackson, William F., and Erika M. Boerman. "Regional heterogeneity in the mechanisms of myogenic tone in hamster arterioles." American Journal of Physiology-Heart and Circulatory Physiology 313, no. 3 (September 1, 2017): H667—H675. http://dx.doi.org/10.1152/ajpheart.00183.2017.
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Myogenic tone is an important feature of arterioles and resistance arteries, but the mechanisms responsible for this hallmark characteristic remain unclear. We used pharmacological inhibitors to compare the roles played by phospholipase C (PLC; 10 μM U73122), inositol 1,4,5-trisphosphate receptors (IP3Rs; 100 μM 2-aminoethoxydiphenylborane), protein kinase C (10 μM bisindolylmaleimide I), angiotensin II type 1 receptors (1 μM losartan), Rho kinase (10 nM−30 μM Y27632 or 300 nM H1152), stretch-activated ion channels (10 nM−1 μM Gd3+ or 5 μM spider venom toxin GsMTx-4) and L-type voltage-gated Ca2+ channels (0.3–100 μM diltiazem) in myogenic tone of cannulated, pressurized (80 cmH2O), second-order hamster cremaster or cheek pouch arterioles. Effective inhibition of either PLC or IP3Rs dilated cremaster arterioles, inhibited Ca2+ waves, and reduced global Ca2+ levels. In contrast, cheek pouch arterioles did not display Ca2+ waves and inhibition of PLC or IP3Rs had no effect on myogenic tone or intracellular Ca2+ levels. Inhibition of Rho kinase dilated both cheek pouch and cremaster arterioles with equal efficacy and potency but also reduced intracellular Ca2+ signals in both arterioles. Similarly, inhibition of mechanosensitive ion channels with Gd2+ or GsMTx-4 produced comparable dilation in both arterioles. Inhibition of L-type Ca2+ channels with diltiazem was more effective in dilating cremaster (86 ± 5% dilation, n = 4) than cheek pouch arterioles (54 ± 4% dilation, n = 6, P < 0.05). Thus, there are substantial differences in the mechanisms underlying myogenic tone in hamster cremaster and cheek pouch arterioles. Regional heterogeneity in myogenic mechanisms could provide new targets for drug development to improve regional blood flow in a tissue-specific manner. NEW & NOTEWORTHY Regional heterogeneity in the mechanisms of pressure-induced myogenic tone implies that resistance vessels may be able to alter myogenic signaling pathways to adapt to their environment. A better understanding of the spectrum of myogenic mechanisms could provide new targets to treat diseases that affect resistance artery and arteriolar function.
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Tykocki, Nathan R., Adrian D. Bonev, Thomas A. Longden, Thomas J. Heppner, and Mark T. Nelson. "Inhibition of vascular smooth muscle inward-rectifier K+ channels restores myogenic tone in mouse urinary bladder arterioles." American Journal of Physiology-Renal Physiology 312, no. 5 (May 1, 2017): F836—F847. http://dx.doi.org/10.1152/ajprenal.00682.2016.
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Prolonged decreases in urinary bladder blood flow are linked to overactive and underactive bladder pathologies. However, the mechanisms regulating bladder vascular reactivity are largely unknown. To investigate these mechanisms, we examined myogenic and vasoactive properties of mouse bladder feed arterioles (BFAs). Unlike similar-sized arterioles from other vascular beds, BFAs failed to constrict in response to increases in intraluminal pressure (5–80 mmHg). Consistent with this lack of myogenic tone, arteriolar smooth muscle cell membrane potential was hyperpolarized (−72.8 ± 1.4 mV) at 20 mmHg and unaffected by increasing pressure to 80 mmHg (−74.3 ± 2.2 mV). In contrast, BFAs constricted to the thromboxane analog U-46619 (100 nM), the adrenergic agonist phenylephrine (10 µM), and KCl (60 mM). Inhibition of nitric oxide synthase or intermediate- and small-conductance Ca2+-activated K+ channels did not alter arteriolar diameter, indicating that the dilated state of BFAs is not attributable to overactive endothelium-dependent dilatory influences. Myocytes isolated from BFAs exhibited BaCl2 (100 µM)-sensitive K+ currents consistent with strong inward-rectifier K+ (KIR) channels. Notably, block of these KIR channels “restored” pressure-induced constriction and membrane depolarization. This suggests that these channels, in part, account for hyperpolarization and associated absence of tone in BFAs. Furthermore, smooth muscle-specific knockout of KIR2.1 caused significant myogenic tone to develop at physiological pressures. This suggests that 1) the regulation of vascular tone in the bladder is independent of pressure, insofar as pressure-induced depolarizing conductances cannot overcome KIR2.1-mediated hyperpolarization; and 2) maintenance of bladder blood flow during bladder filling is likely controlled by neurohumoral influences.
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Huang, An, and Akos Koller. "Endothelin and Prostaglandin H2Enhance Arteriolar Myogenic Tone in Hypertension." Hypertension 30, no. 5 (November 1997): 1210–15. http://dx.doi.org/10.1161/01.hyp.30.5.1210.
Full textDissertations / Theses on the topic "Arteriolar myogenic tone"
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Raina, Hema, and hemaraina@yahoo com. "Functional significance of sodium calcium exchange in arteriolar myogenic zone." RMIT University. Medical Sciences, 2006. http://adt.lib.rmit.edu.au/adt/public/adt-VIT20080812.155348.
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To determine a possible role for NCX in myogenically active smooth muscle arterioles, studies were conducted by manipulation of extracellular Na+ levels and inhibition of the exchanger. Western blotting was performed for the identification of the NCX protein. Real-time PCR was performed to demonstrate the level of expression of mRNA, for the NCX isoforms. Antisense oligonucleotides against NCX mRNA were introduced in an isolated cremaster arteriole followed by functional studies after 24 hours. Level of expression of NCX was determined by western blotting. The data are consistent with the presence of NCX1 in the cremaster arterioles.
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Li, Yao. "Contributions of TRPM4 and Rho Kinase to Myogenic Tone Development in Cerebral Parenchymal Arterioles." ScholarWorks @ UVM, 2016. http://scholarworks.uvm.edu/graddis/464.
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Cerebral parenchymal arterioles (PAs) play a critical role in assuring appropriate blood flow and perfusion pressure within the brain. PAs are unique in contrast to upstream pial arteries, as defined by their critical roles in neurovascular coupling, distinct sensitivities to vasoconstrictors, and enhanced myogenic responsiveness. Dysfunction of these blood vessels is implicated in numerous cardiovascular diseases. However, treatments are limited due to incomplete understanding of the fundamental control mechanisms at this level of the circulation. One of the key elements within most vascular networks, including the cerebral circulation, is the presence of myogenic tone, an intrinsic process whereby resistance arteries constrict and reduce their diameter in response to elevated arterial pressure. This process is centrally involved in the ability of the brain to maintain nearly constant blood flow over a broad range of systemic blood pressures. The overall goal of this dissertation was to investigate the unique mechanisms of myogenic tone regulation in the cerebral microcirculation. To reveal the contributions of various signaling factors in this process, measurements of diameter, intracellular Ca2+ concentration ([Ca2+]i), membrane potential and ion channel activity were performed. Initial work determined that two purinergic G protein-coupled receptors, P2Y4 and P2Y6 receptors, play a unique role in mediating pressure-induced vasoconstriction of PAs in a ligand-independent manner. Moreover, a particular transient receptor potential (TRP) channel in the melastatin subfamily, i.e. TRPM4, was also identified as a mediator of PA myogenic responses. Notably, the observations that inhibiting TRPM4 channels substantially reduces P2Y receptor-mediated depolarization and vasoconstriction, and that P2Y receptor ligands markedly activate TRPM4 currents provide definitive evidence that this ion channel functions as an important link between mechano-sensitive P2Y receptor activation and the myogenic response in PAs. Next, the signaling cascades that mediate stretch-induced TRPM4 activation in PA myocytes were explored. Interestingly, these experiments determined that the RhoA/Rho kinase signaling pathway is involved in this mechanism by facilitating pressure-induced, P2Y receptor-mediated stimulation of TRPM4 channels, leading to subsequent smooth muscle depolarization, [Ca2+]i increase and contraction. Since Rho kinase is generally accepted as a 'Ca2+-sensitization' mediator, the present, contrasting observations point to an underappreciated role of RhoA/Rho kinase signaling in the excitation-contraction mechanisms within the cerebral microcirculation. Overall, this dissertation provides evidence that myogenic regulation of cerebral PAs is mediated by mechano-sensitive P2Y receptors, which initiate the RhoA/Rho kinase signaling pathway, subsequent TRPM4 channel opening, and concomitant depolarization and contraction of arteriolar smooth muscle cells. Revealing the unique mechanochemical coupling mechanisms in the cerebral microcirculation may lead to development of innovative therapeutic strategies for prevention and treatment of microvascular pathologies in the brain.
Book chapters on the topic "Arteriolar myogenic tone"
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Jackson, William F. "Ion channels and the regulation of myogenic tone in peripheral arterioles." In Current Topics in Membranes, 19–58. Elsevier, 2020. http://dx.doi.org/10.1016/bs.ctm.2020.01.002.
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Gielen, Stephan, M. Harold Laughlin, and Dirk J. Duncker. "Vascular remodelling." In The ESC Textbook of Sports Cardiology, edited by Antonio Pelliccia, Hein Heidbuchel, Domenico Corrado, Mats Börjesson, and Sanjay Sharma, 41–48. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198779742.003.0005.
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Vascular remodelling plays an important role in the adaptation of the athlete to increased exercise duration and intensity. Endurance exercise improves endothelium-dependent flow-mediated vasodilation and leads to increases in conduit artery lumen diameter after regular exercise, typically in the trained limb. These changes result in a reduced vascular stiffnes. On the contrary strength training (e.g. for weight-lifting) produces increased vascular stiffness and enlarged central vessels (e.g. aortic root diameters), while the diameters of peripheral vessels are unchanged. In the skeletal muscle, endurance training increases capillary density and improves oxygen exchange, thus adding further functional reserves to the aerobic exercise capacity. Aerobic exercise leads to a large increase in cardiac functional reserves, hence myocardial perfusion is increased in line with metabolic demands. In addition to improved endothelium-dependent vasodilation, coronary arterioles also exhibit an increased myogenic tone.