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1
Vatta, M. S., L. G. Bianciotti, A. S. Locatelli, M. L. Papouchado, and B. E. Fernández. "Monophasic and biphasic effects of angiotensin II and III on norepinephrine uptake and release in rat adrenal medulla." Canadian Journal of Physiology and Pharmacology 70, no. 6 (June 1, 1992): 821–25. http://dx.doi.org/10.1139/y92-110.
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Angiotensin II and III have hypertensive effects. They induce vascular smooth muscle constriction, increase sodium reabsorption by renal tubules, stimulate the anteroventral third ventricle area, increase vasopressin and aldosterone secretions, and modify catecholamine metabolism. In this work, angiotensin II and III effects on norepinephrine uptake and release in rat adrenal medulla were investigated. Both angiotensins decreased total and neuronal norepinephrine uptake. Angiotensin II showed a biphasic effect only on evoked neuronal norepinephrine release (an earlier decrease followed by a later increase), while increasing the spontaneous norepinephrine release only after 12 min. On the other hand, angiotensin III showed a biphasic effect on evoked and spontaneous neuronal norepinephrine release. Both angiotensins altered norepinephrine distribution into intracellular stores, concentrating the amine into the granular pool and decreasing the cytosolic store. The results suggest a physiological biphasic effect of angiotensin II as well as angiotensin III that may be involved in the modulation of sympathetic activity in the rat adrenal medulla.Key words: angiotensin II, angiotensin III, norepinephrine uptake, norepinephrine release, adrenal medulla.
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Lin, K. S., J. Y. Chan, and S. H. Chan. "Involvement of AT2 receptors at NRVL in tonic baroreflex suppression by endogenous angiotensins." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 5 (May 1, 1997): H2204—H2210. http://dx.doi.org/10.1152/ajpheart.1997.272.5.h2204.
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We evaluated the role of endogenous angiotensin II and III (ANG II and ANG III) at the rostral nucleus reticularis ventrolateralis (NRVL) in the modulation of baroreceptor reflex (BRR) response and the subtype of angiotensin receptors involved in this process. Adult male Sprague-Dawley rats anesthetized and maintained with pentobarbital sodium were used. Exogenous application of ANG II or ANG III (10, 20, or 40 pmol) by bilateral microinjection into the NRVL significantly suppressed the BRR response to transient hypertension induced by phenylephrine (5 micrograms/kg i.v.). The suppressive effect of ANG II (20 pmol) was reversed by an equimolar dose (1.6 nmol) of its peptide antagonist, [Sar1, Ile8]ANG II, and the nonpeptide antagonists for AT1 and AT2 receptors, losartan and PD-123319, respectively. On the other hand, the inhibitory action of ANG III (20 pmol) was blunted by its peptide antagonist. [Ile7]ANG III or PD-123319, but not by losartan. Blocking the endogenous activity of the angiotensins by microinjection into the bilateral NRVL of [Sar1, Ile8]ANG II, [Ile7]ANG III, or PD-123319 elicited an appreciable enhancement of the BRR response, whereas losartan produced minimal effect. These results suggest that, under physiological conditions, both endogenous ANG II and ANG III may exert a tonic inhibitory modulation on the BRR response by acting selectively on the AT2 receptors at the NRVL.
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Mezei, Za, Á. Gecse, and G. Telegdy. "The effect of angiotensins on the arachidonate cascade of rat brain microvessels and platelets." International Journal of Psychophysiology 7, no. 2-4 (August 1989): 315–17. http://dx.doi.org/10.1016/0167-8760(89)90253-5.
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Lancien, Frédéric, Marty Wong, Ali Al Arab, Nagi Mimassi, Yoshio Takei, and Jean-Claude Le Mével. "Central ventilatory and cardiovascular actions of angiotensin peptides in trout." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 303, no. 3 (August 1, 2012): R311—R320. http://dx.doi.org/10.1152/ajpregu.00145.2012.
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In the brains of teleosts, angiotensin II (ANG II), one of the main effector peptides of the renin-angiotensin system, is implicated in various physiological functions notably body fluid and electrolyte homeostasis and cardiovascular regulation, but nothing is known regarding the potential action of ANG II and other angiotensin derivatives on ventilation. Consequently, the goal of the present study was to determine possible ventilatory and cardiovascular effects of intracerebroventricular injection of picomole doses (5–100 pmol) of trout [Asn1]-ANG II, [Asp1]-ANG II, ANG III, ANG IV, and ANG 1–7 into the third ventricle of unanesthetized trout. The central actions of these peptides were also compared with their ventilatory and cardiovascular actions when injected peripherally. Finally, we examined the presence of [Asn1]-ANG II, [Asp1]-ANG II, ANG III, and ANG IV in the brain and plasma using radioimmunoassay coupled with high-performance liquid chromatography. After intracerebroventricular injection, [Asn1]-ANG II and [Asp1]-ANG II two ANG IIs, elevated the total ventilation through a selective stimulatory action on the ventilation amplitude. However, the hyperventilatory effect of [Asn1]-ANG II was threefold higher than the effect of [Asp1]-ANG II at the 50-pmol dose. ANG III, ANG IV, and ANG 1–7 were without effect. In addition, ANG IIs and ANG III increased dorsal aortic blood pressure (PDA) and heart rate (HR). After intra-arterial injections, none of the ANG II peptides affected the ventilation but [Asn1]-ANG II, [Asp1]-ANG II, and ANG III elevated PDA (50 pmol: +80%, +58% and +48%, respectively) without significant decrease in HR. In brain tissue, comparable amounts of [Asn1]-ANG II and [Asp1]-ANG II were detected (ca. 40 fmol/mg brain tissue), but ANG III was not detected, and the amount of ANG IV was about eightfold lower than the content of the ANG IIs. In plasma, ANG IIs were also the major angiotensins (ca. 110 fmol/ml plasma), while significant but lower amounts of ANG III and ANG IV were present in plasma. In conclusion, our study suggests that the two ANG II isoforms produced within the brain may act as a neurotransmitter and/or neuromodulator to regulate the cardioventilatory functions in trout. In the periphery, two ANG IIs and their COOH-terminal peptides may act as a circulating hormone preferentially involved in cardiovascular regulations.
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McGiff, John C., and John Quilley. "20-HETE and the kidney: resolution of old problems and new beginnings." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 277, no. 3 (September 1, 1999): R607—R623. http://dx.doi.org/10.1152/ajpregu.1999.277.3.r607.
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The protean properties of 20-hydroxyeicosatetraenoic acid (HETE), vasoactivity, mitogenicity, and modulation of transport in key nephron segments, serve as the basis for the essential roles of 20-HETE in the regulation of the renal circulation and electrolyte excretion and as a second messenger for endothelin-1 and mediator of selective renal effects of ANG II. Renal autoregulation and tubular glomerular feedback are mediated by 20-HETE through constriction of preglomerular arterioles, responses that are maintained by 20-HETE inhibition of calcium-activated potassium channels. 20-HETE modulates ion transport in the proximal tubules and the thick ascending limb by affecting the activities of Na+-K+-ATPase and the Na+-K+-2Cl−cotransporter, respectively. The range and diversity of activity of 20-HETE derives in large measure from COX-dependent transformation of 20-HETE to products affecting vasomotion and salt and water excretion. Nitric oxide (NO) exerts a negative modulatory effect on 20-HETE formation; inhibition of NO synthesis produces marked perturbation of renal function resulting from increased 20-HETE production. 20-HETE is an essential component of interactions involving several hormonal systems that have central roles in blood pressure homeostasis, including angiotensins, endothelins, NO, and cytokines. 20-HETE is the preeminent renal eicosanoid, overshadowing PGE2 and PGI2. This review is intended to provide evidence for the physiological roles for cytochrome P-450-derived eicosanoids, particularly 20-HETE, and seeks to extend this knowledge to a conceptual framework for overall cardiovascular function.
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Jutte, Sara B., and Jon E. Sprague. "Pharmacologic Regulation of the Renin—Angiotensin System: Physiologic and Pathologic Effects." Journal of Pharmacy Technology 16, no. 4 (July 2000): 138–46. http://dx.doi.org/10.1177/875512250001600408.
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Objective: To review the physiologic and pathologic roles of the renin-angiotensin system in maintaining blood pressure, glomerular filtration rate, and myocardial tissue growth. The pharmacologic regulations of the pathologic effects of the renin-angiotensin system are emphasized, with a comparison between angiotensin-converting enzyme (ACE) inhibitors and angiotensin1 receptor (AT1) antagonists. Data Sources: English-language basic science, clinical studies, and review articles were identified using MEDLINE, IOWA, and a manual search from January 1966 through September 1999. References were also obtained from the reference section of relevant published articles. Study Selection and Data Extraction: All articles identified were evaluated for possible inclusion in this review. Evaluative and comparative data from basic science and controlled clinical studies were reviewed. Data Synthesis: The renin-angiotensin system has a plethora of physiologic and pathologic roles in the regulation of blood pressure, renal function, and cell growth. The cellular mechanisms involved in eliciting the responses to the renin-angiotensin system are discussed in detail, with an emphasis on the pharmacologic regulation of the cellular responses. The role of angiotensin II in maintaining blood pressure, glomerular filtration rate, and in regulating myocardial cell growth secondary to myocardial infarction or as a complication of congestive heart failure are all reviewed. The ACE inhibitors and AT1 antagonists have comparable pharmacologic effects that can influence their therapeutic application. The ACE inhibitors and AT, antagonists are compared regarding clinically and experimentally observed differences that may affect their therapeutic application. Conclusions: The physiologic and pathologic roles of the renin-angiotensin system make the ACE inhibitors and AT1 antagonists ideal candidates in treating many conditions. Presently, few studies have been conducted that directly compare ACE inhibitors and AT, antagonists. An understanding of the basic underlying pharmacologic principles is essential when attempting to apply the scientific and clinical information of the ACE inhibitors and AT1 antagonists with the intention of extrapolating to therapeutic utility.
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Tolessa, Debela, Adugna Chala, Kelil Haji, Gizaw Mamo, and Gizaw Eshetu. "Physiological Effects of Angiotensin III." International Journal of Clinical and Experimental Physiology 5, no. 4 (December 30, 2019): 164–67. http://dx.doi.org/10.5530/ijcep.2018.5.4.15.
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Evered, Mark D. "Investigating the role of angiotensin II in thirst: Interactions between arterial pressure and the control of drinking." Canadian Journal of Physiology and Pharmacology 70, no. 5 (May 1, 1992): 791–97. http://dx.doi.org/10.1139/y92-105.
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Several lines of evidence suggest that angiotensin II plays a physiological role in the control of thirst. Establishing that, however, has been surprisingly difficult, given our current knowledge about the renin–angiotensin systems in the circulation and the brain and the variety of techniques available to measure and manipulate them. A major problem is that stimulating or blocking the renin–angiotensin system affects several physiological variables simultaneously. Since several of these variables also influence the controls of water intake directly or indirectly, the interpretation of the effect on drinking becomes more difficult. To illustrate the problem and recent developments, this paper describes some of the interactions between the effects of angiotensin II on arterial pressure and thirst, and it shows how they have contributed to the controversy over the physiological role of the peptide.Key words: renin–angiotensin system, thirst, arterial pressure.
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Fernando, K. C., and G. J. Barritt. "Evidence from studies with hepatocyte suspensions that store-operated Ca2+ inflow requires a pertussis toxin-sensitive trimeric G-protein." Biochemical Journal 303, no. 2 (October 15, 1994): 351–56. http://dx.doi.org/10.1042/bj3030351.
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The role of heterotrimeric GTP-binding proteins in the process of store-operated Ca2+ inflow in hepatocytes was investigated by testing the ability of pertussis toxin to inhibit thapsigargin- and 2,5-di-tert-butylhydroquinone (DBHQ)-induced bivalent cation inflow. Hepatocytes isolated from rats treated with pertussis toxin for 24 h exhibited markedly inhibited rates of both Ca2+ and Mn2+ inflow when these were stimulated by vasopressin, angiotension II, epidermal growth factor, thapsigargin and DBHQ. Pertussis toxin had little effect on the basal intracellular free Ca2+ concentration ([Ca2+]i), basal rates of Ca2+ and Mn2+ inflow, the abilities of vasopressin, angiotensin II, thapsigargin and DBHQ to induce the release of Ca2+ from intracellular stores, and the maximum value of [Ca2+]i reached following agonist-induced release of Ca2+ from intracellular stores. It is concluded that store-operated Ca2+ inflow in hepatocytes employs a slowly ADP-ribosylated trimeric GTP-binding protein and is the physiological mechanism, or one of the physiological mechanisms, by which vasopressin and angiotensin stimulate plasma membrane Ca2+ inflow in this cell type.
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Leal, Marcos André Soares, Thanisia de Almeida, João Guilherme Torres, Luciene Cristina Gastalho Campos, Elisardo Corral Vasquez, and Valério Garrone Barauna. "Physiological and Biochemical Vascular Reactivity Parameters of Angiotensin II and the Action of Biased Agonist TRV023." Advances in Pharmacological and Pharmaceutical Sciences 2020 (March 1, 2020): 1–8. http://dx.doi.org/10.1155/2020/3092721.
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Vascular reactivity experiments using isolated aortic rings have been widely used as a model for physiological and pharmacological studies since the early sixties. Here, we suggest several parameters that the researcher should pay attention to when investigating angiotensin II in their experimental models. Angiotensin II is one of the active peptides of the renin-angiotensin system and exerts its effect through the AT1 and AT2 receptors. Some studies seek to understand the effects of angiotensin II receptors at the vascular level by using vascular reactivity experiments. However, because of the large number of variations, there are only a handful of reactivity studies that seek to use this method. Thus, the objective of this study was to standardize experimental methods with angiotensin II, through vascular reactivity protocols. For this, variables such as basal tension, concentration interval, single concentration, curve concentration response, and multiple experiments using the same aortic ring were developed using the technique of vascular reactivity in an organ bath. This is the first study that has standardized the vascular reactivity protocol. In addition, we demonstrated the effects of TRV023-biased ligand of the AT1R at vascular sites.
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Sechi, L. A., E. F. Grady, C. A. Griffin, J. E. Kalinyak, and M. Schambelan. "Distribution of angiotensin II receptor subtypes in rat and human kidney." American Journal of Physiology-Renal Physiology 262, no. 2 (February 1, 1992): F236—F240. http://dx.doi.org/10.1152/ajprenal.1992.262.2.f236.
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Angiotensin II initiates a variety of physiological effects in the kidney by binding to high-affinity receptors on plasma membranes. Recently, two subtypes of angiotensin II receptors have been distinguished on the basis of differences in signal transduction mechanisms, binding affinity to agonists and antagonists, and inhibition of binding by dithiothreitol. To evaluate the density and distribution of these receptor subtypes in the kidney, we performed an in situ autoradiographic study on frozen tissue sections obtained from rat and human kidneys. Sections were incubated with 125I-[Sar1,Ile8]angiotensin II and binding specificity was verified by competition with unlabeled [Sar1]angiotensin II. Angiotensin II receptor subtypes were characterized by competition with the nonpeptide receptor antagonists, DuP 753 (type 1) and PD123177 (type 2). Both rat and human kidney exhibited a high concentration of angiotensin II receptors in glomeruli and in the longitudinal bands traversing the outer portion of the medulla, corresponding to the medullary vascular bundles. Binding affinity (Kd = 0.6 +/- 0.4 nM), determined in rat kidney, was similar to that reported previously in isolated glomeruli and membrane vesicles prepared from renal tubules. Angiotensin II binding was almost completely inhibited by DuP 753, whereas PD123177 had little effect. Thus the predominant angiotensin II receptor subtype in both rat and human kidney is type 1. The distribution of angiotensin II receptors correlates well with the intrarenal sites at which the peptide has its major physiological effects.
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Ferrario, C. M., M. C. Chappell, R. H. Dean, and S. N. Iyer. "Novel angiotensin peptides regulate blood pressure, endothelial function, and natriuresis." Journal of the American Society of Nephrology 9, no. 9 (September 1998): 1716–22. http://dx.doi.org/10.1681/asn.v991716.
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Accumulating evidence suggests that angiotensin-(1-7) is an important component of the renin-angiotensin system, having actions that are either identical to or opposite that of angiotensin II. Angiotensin I can be directly converted to angiotensin-(1-7), bypassing formation of angiotensin II. This pathway is under the control of three enzymes: neutral endopeptidases 24.11 (neprilysin) and 24.15 and prolyl-endopeptidase 24.26. Two of the three angiotensin-forming enzymes (neprilysin and endopeptidase 24.15) also contribute to the breakdown of bradykinin and the atrial natriuretic peptide. Furthermore, angiotensin-(1-7) is a major substrate for angiotensin-converting enzyme. These observations suggest that the process of biotransformation between the various Ang peptides of the renin-angiotensin system and other vasodepressor peptides are intertwined through this enzymatic pathway. Substantial evidence suggests that angiotensin-(1-7) stimulates the synthesis and release of vasodilator prostaglandins, and nitric oxide, while also augmenting the metabolic actions of bradykinin. In addition, angiotensin-(1-7) alters tubular sodium and bicarbonate reabsorption, decreases Na+-K+-ATPase activity, induces diuresis, and exerts a vasodilator effect. These physiologic effects of angiotensin-(1-7) favor a blood pressure-lowering effect. The majority of the data currently available suggest that angiotensin-(1-7) mediates its effects through a novel non-AT1/AT2 receptor subtype.
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Kato, Akihiko, Janet D. Klein, Chi Zhang, and Jeff M. Sands. "Angiotensin II increases vasopressin-stimulated facilitated urea permeability in rat terminal IMCDs." American Journal of Physiology-Renal Physiology 279, no. 5 (November 1, 2000): F835—F840. http://dx.doi.org/10.1152/ajprenal.2000.279.5.f835.
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Angiotensin II receptors are present along the rat inner medullary collecting duct (IMCD), although their physiological role is unknown. Because urea is one of the major solutes transported across the terminal IMCD, we measured angiotensin II's effect on urea permeability. In the perfused rat terminal IMCD, angiotensin II had no effect on basal urea permeability but significantly increased vasopressin-stimulated urea permeability by 55%. Angiotensin II, both without and with vasopressin, also increased the amount of 32P incorporated into urea transporter (UT)-A1 in inner medullary tissue exposed to these hormones ex vivo. Because angiotensin II activates protein kinase C, we tested the effect of staurosporine (SSP). In the absence of angiotensin II, SSP had no effect on vasopressin-stimulated urea permeability in the perfused terminal IMCD. However, SSP completely and reversibly blocked the angiotensin II-mediated increase in vasopressin-stimulated urea permeability. SSP and chelerythrine reduced the angiotensin II-stimulated 32P incorporation into UT-A1 in inner medullary tissue exposed ex vivo. We conclude that angiotensin II increases vasopressin-stimulated facilitated urea permeability and32P incorporation into the 97- and 117-kDa UT-A1 proteins via a protein kinase C-mediated signaling pathway. These data suggest that angiotensin II augments vasopressin-stimulated facilitated urea transport in the rat terminal IMCD and may play a physiological role in the urinary concentrating mechanism by augmenting the maximal response to vasopressin.
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DiBona, Gerald F., and Linda L. Sawin. "Effect of endogenous angiotensin II on the frequency response of the renal vasculature." American Journal of Physiology-Renal Physiology 287, no. 6 (December 2004): F1171—F1178. http://dx.doi.org/10.1152/ajprenal.00201.2004.
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The renal vasculature functions as an efficient low-pass filter of the multiple frequencies contained within renal sympathetic nerve activity. This study examined the effect of angiotensin II on the frequency response of the renal vasculature. Physiological changes in the activity of the endogenous renin-angiotensin system were produced by alterations in dietary sodium intake. The frequency response of the renal vasculature was evaluated using pseudorandom binary sequence renal nerve stimulation, and the role of angiotensin II was evaluated by the administration of the angiotensin II AT1-receptor antagonist losartan. In low-sodium-diet rats with increased renin-angiotensin system activity, losartan steepened the renal vascular frequency response (i.e., greater attenuation); this was not seen in normal- or high-sodium-diet rats with normal or decreased renin-angiotensin system activity. Analysis of the transfer function from arterial pressure to renal blood flow, i.e., dynamic autoregulation, showed that the tubuloglomerular feedback but not the myogenic component was enhanced in low- and normal- but not in high-sodium-diet rats and that this was reversed by losartan administration. Thus physiological increases in endogenous renin-angiotensin activity inhibit the renal vascular frequency response to renal nerve stimulation while selectively enhancing the tubuloglomerular feedback component of dynamic autoregulation of renal blood flow.
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Kim, Il-Sup, Woong-Suk Yang, and Cheorl-Ho Kim. "Beneficial Effects of Soybean-Derived Bioactive Peptides." International Journal of Molecular Sciences 22, no. 16 (August 9, 2021): 8570. http://dx.doi.org/10.3390/ijms22168570.
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Peptides present in foods are involved in nutritional functions by supplying amino acids; sensory functions related to taste or solubility, emulsification, etc.; and bioregulatory functions in various physiological activities. In particular, peptides have a wide range of physiological functions, including as anticancer agents and in lowering blood pressure and serum cholesterol levels, enhancing immunity, and promoting calcium absorption. Soy protein can be partially hydrolyzed enzymatically to physiologically active soy (or soybean) peptides (SPs), which not only exert physiological functions but also help amino acid absorption in the body and reduce bitterness by hydrolyzing hydrophobic amino acids from the C- or N-terminus of soy proteins. They also possess significant gel-forming, emulsifying, and foaming abilities. SPs are expected to be able to prevent and treat atherosclerosis by inhibiting the reabsorption of bile acids in the digestive system, thereby reducing blood cholesterol, low-density lipoprotein, and fat levels. In addition, soy contains blood pressure-lowering peptides that inhibit angiotensin-I converting enzyme activity and antithrombotic peptides that inhibit platelet aggregation, as well as anticancer, antioxidative, antimicrobial, immunoregulatory, opiate-like, hypocholesterolemic, and antihypertensive activities. In animal models, neuroprotective and cognitive capacity as well as cardiovascular activity have been reported. SPs also inhibit chronic kidney disease and tumor cell growth by regulating the expression of genes associated with apoptosis, inflammation, cell cycle arrest, invasion, and metastasis. Recently, various functions of soybeans, including their physiologically active functions, have been applied to health-oriented foods, functional foods, pharmaceuticals, and cosmetics. This review introduces some current results on the role of bioactive peptides found in soybeans related to health functions.
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Nagami, G. T. "Effect of luminal angiotensin II on ammonia production and secretion by mouse proximal tubules." American Journal of Physiology-Renal Physiology 269, no. 1 (July 1, 1995): F86—F92. http://dx.doi.org/10.1152/ajprenal.1995.269.1.f86.
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Angiotensin II is an important regulator of acid-base and ammonia metabolism in the proximal tubule. Because angiotensin II receptors exist on the apical membrane and because luminal fluid angiotensin II concentrations may be substantial, the effects of luminal angiotensin II on ammonia production rates and net luminal total ammonia (tNH3) secretion rates were examined in dissected mouse S2 proximal tubule segments. Ammonia production rates reflected the total release of ammonia via the basolateral and luminal aspects of the tubule, whereas net luminal secretion rates reflected the rates at which ammonia left the tubule via the luminal fluid leaving the distal end of the perfused segment. The results demonstrated that 1) luminal angiotensin II affected tNH3 production in a concentration-dependent fashion, 2) luminal angiotensin II at concentrations that stimulated tNH3 production could counteract the effect of inhibitory basolateral concentrations of angiotensin II, 3) the stimulation of tNH3 production and the rise in intracellular calcium concentration induced by 10(-10) M luminal angiotensin II were blocked by the addition of an angiotensin II receptor inhibitor, saralasin, or the calcium channel blocker nifedipine to the luminal perfusion solution, and 4) in contrast to basolateral angiotensin II, which inhibited net luminal tNH3 secretion, luminal angiotensin II stimulated amiloride-sensitive net luminal tNH3 secretion in parallel with stimulation of luminal fluid acidification. Thus luminal angiotensin II at physiological and superphysiological concentrations has important effects on ammonia production and transport in the proximal tubule that in some ways differ from the effects of basolateral angiotensin II.
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Phillips, P. A., B. J. Rolls, J. G. G. Ledingham, J. J. Morton, and M. L. Forsling. "Angiotensin II-induced thirst and vasopressin release in man." Clinical Science 68, no. 6 (June 1, 1985): 669–74. http://dx.doi.org/10.1042/cs0680669.
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1. The thirst and plasma vasopressin responses to single-blind controlled intravenous angiotensin II infusions (2-16 ng min−1 kg−1) were investigated in ten healthy young men. 2. Thirst and vasopressin secretion were stimulated in four out of ten subjects. These effects occurred at plasma angiotensin concentrations well above those measured under physiological conditions associated with thirst and vasopressin secretion such as water deprivation. 3. Further studies are needed to define why only certain individuals respond to intravenous angiotensin II infusions and to determine whether potentiation of angiotensin-induced thirst and vasopressin secretion by other stimuli (e.g. hypovolaemia and hypertonicity) might occur in man, in particular under pathological conditions when plasma angiotensin levels are above the physiological range.
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Mehta, Puja K., and Kathy K. Griendling. "Angiotensin II cell signaling: physiological and pathological effects in the cardiovascular system." American Journal of Physiology-Cell Physiology 292, no. 1 (January 2007): C82—C97. http://dx.doi.org/10.1152/ajpcell.00287.2006.
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The renin-angiotensin system is a central component of the physiological and pathological responses of cardiovascular system. Its primary effector hormone, angiotensin II (ANG II), not only mediates immediate physiological effects of vasoconstriction and blood pressure regulation, but is also implicated in inflammation, endothelial dysfunction, atherosclerosis, hypertension, and congestive heart failure. The myriad effects of ANG II depend on time (acute vs. chronic) and on the cells/tissues upon which it acts. In addition to inducing G protein- and non-G protein-related signaling pathways, ANG II, via AT1 receptors, carries out its functions via MAP kinases (ERK 1/2, JNK, p38MAPK), receptor tyrosine kinases [PDGF, EGFR, insulin receptor], and nonreceptor tyrosine kinases [Src, JAK/STAT, focal adhesion kinase (FAK)]. AT1R-mediated NAD(P)H oxidase activation leads to generation of reactive oxygen species, widely implicated in vascular inflammation and fibrosis. ANG II also promotes the association of scaffolding proteins, such as paxillin, talin, and p130Cas, leading to focal adhesion and extracellular matrix formation. These signaling cascades lead to contraction, smooth muscle cell growth, hypertrophy, and cell migration, events that contribute to normal vascular function, and to disease progression. This review focuses on the structure and function of AT1 receptors and the major signaling mechanisms by which angiotensin influences cardiovascular physiology and pathology.
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de Resende, Micheline M., Sandra L. Amaral, Carol Moreno, and Andrew S. Greene. "Congenic strains reveal the effect of the renin gene on skeletal muscle angiogenesis induced by electrical stimulation." Physiological Genomics 33, no. 1 (March 2008): 33–40. http://dx.doi.org/10.1152/physiolgenomics.00150.2007.
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Previous studies have indicated the importance of angiotensin II (ANG II) in skeletal muscle angiogenesis. The present study explored the effect of regulation of the renin gene on angiogenesis induced by electrical stimulation with the use of physiological, pharmacological, and genetic manipulations of the renin-angiotensin system (RAS). Transfer of the entire chromosome 13, containing the physiologically regulated renin gene, from the normotensive inbred Brown Norway (BN) rat into the background of an inbred substrain of the Dahl salt-sensitive (SS/Mcwi) rat restored renin levels and the angiogenic response after electrical stimulation. This restored response was significantly attenuated when SS-13BN/Mcwi consomic rats were treated with lisinopril or high-salt diet. The role of ANG II on this effect was confirmed by the complete restoration of skeletal muscle angiogenesis in SS/Mcwi rats infused with subpressor doses of ANG II. Congenic strains derived from the SS-13BN/Mcwi consomic were used to further verify the role of the renin gene in this response. Microvessel density was markedly increased after stimulation in congenic strains that contained the renin gene from the BN rat (congenic lines A and D). This angiogenic response was suppressed in control strains that carried regions of the BN genome just above (congenic line C) or just below (congenic line B) the renin gene. The present study emphasizes the importance of maintaining normal renin regulation as well as ANG II levels during the angiogenesis process with a combination of physiological, genetic, and pharmacological manipulation of the RAS.
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Sica, Domenic A. "Angiotensin‐Converting Enzyme Inhibitors' Side Effects—Physiologic and Non‐Physiologic Considerations." Journal of Clinical Hypertension 7, s8 (August 2005): 17–23. http://dx.doi.org/10.1111/j.1524-6175.2005.04556.x.
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Grace, A. A., J. C. Metcalfe, P. L. Weissberg, H. W. Bethell, and J. I. Vandenberg. "Angiotensin II stimulates sodium-dependent proton extrusion in perfused ferret heart." American Journal of Physiology-Cell Physiology 270, no. 6 (June 1, 1996): C1687—C1694. http://dx.doi.org/10.1152/ajpcell.1996.270.6.c1687.
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The Na+/H+ antiport and Na(+)-HCO3- coinflux carrier contribute to recovery from intracellular acidosis in cardiac tissue. The effects of angiotensin II (10(-12)-10(-6) M) on H+ fluxes after intracellular acid loading and during reperfusion after myocardial ischemia have been investigated in the isovolumic, Langendorff-perfused ferret heart. Intracellular pH (pHi) was estimated using 31P nuclear magnetic resonance (NMR) spectroscopy from the chemical shift of intracellular deoxyglucose-6-phosphate or inorganic phosphate. Angiotensin II produced concentration-dependent stimulation (maximum at 10(-6) M: 67%) of 5-(N-ethyl-N-isopropyl)amiloride (EIPA)-sensitive Na(+)-dependent of H+ efflux consistent with stimulation of the Na+/H+ antiport. Half-maximal stimulation of H+ efflux occurred at approximately 10(-9) M, which is close to the dissociation constant of the cardiac angiotensin AT1 receptor. Stimulation via this receptor was confirmed with the nonpeptide AT1 receptor blocker, GR-117289. Angiotensin II had less pronounced effects on HCO3(-)-dependent pHi recovery after acid loading with no effect on pHi recovery after intracellular alkalosis. During reperfusion, angiotensin II significantly increased H+ extrusion but impaired contractile recovery. The results support the hypothesis that angiotensin II facilitates H+ extrusion in the heart. This may help maintain physiological homeostasis, but the hypothesized obligated Na+ influx could exacerbate cellular dysfunction during reperfusion.
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Schiffrin, Ernesto L., Douglas J. Franks, and Jolanta Gutkowska. "Effect of aldosterone on vascular angiotensin II receptors in the rat." Canadian Journal of Physiology and Pharmacology 63, no. 12 (December 1, 1985): 1522–27. http://dx.doi.org/10.1139/y85-250.
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The effect of aldosterone on the density and affinity of binding sites for 125I-labelled angiotensin II was investigated in a particulate fraction prepared from the rat mesenteric arteriolar arcades. The infusion of aldosterone 6.6 μg/h intraperitoneally via Alzet osmotic minipumps for 6 d produced an increase in the density of binding sites for 125I-labelled angiotensin II without change in affinity. After sodium depletion, mesenteric artery angiotensin II receptors were down-regulated as expected. An increase in the number of binding sites could be found when aldosterone was infused into sodium-depleted rats with no change in the elevated plasma renin activity. The intraperitoneal infusion of angiotensin II (200 ng ∙ kg−1 ∙ min−1 for 6 d) simultaneously with aldosterone resulted in down-regulation of vascular angiotensin II receptors, whereas after intravenous angiotensin II infusion (at 60 ng ∙ kg−1 ∙ min−1) the density of angiotensin II binding sites rose with aldosterone infusion. Plasma renin activity (PRA) was reduced and plasma angiotensin II increased in a dose-dependent fashion after angiotensin II infusion. An aldosterone concentration of 3 ng/mL for 18 h produced an increase in the number of angiotensin II binding sites in rat mesenteric artery smooth muscle cells in culture. We conclude that increased plasma aldosterone may result in up-regulation of vascular angiotensin II receptors independently of changes in plasma renin activity, and may in certain physiological states effectively antagonize the down-regulating action of angiotensin II.
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Plovsing, Ronni R., Christian Wamberg, Niels C. F. Sandgaard, Jane A. Simonsen, Niels-Henrik Holstein-Rathlou, Poul Flemming Høilund-Carlsen, and Peter Bie. "Effects of truncated angiotensins in humans after double blockade of the renin system." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 285, no. 5 (November 2003): R981—R991. http://dx.doi.org/10.1152/ajpregu.00263.2003.
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Angiotensins different from ANG II exhibit biological activities, possibly mediated via receptors other than ANG II receptors. We studied the effects of 3-h infusions of ANG III, ANG-(1-7), and ANG IV in doses equimolar to physiological amounts of ANG II (3 pmol · kg-1 · min-1), in six men on low-sodium diet (30 mmol/day). The subjects were acutely pretreated with canrenoate and captopril to inhibit aldosterone actions and ANG II synthesis, respectively. ANG II infusion increased plasma angiotensin immunoreactivity to 53 ± 6 pg/ml (+490%), plasma aldosterone to 342 ± 38 pg/ml (+109%), and blood pressure by 27%. Glomerular filtration rate decreased by 16%. Concomitantly, clearance of endogenous lithium fell by 66%, and fractional proximal reabsorption of sodium increased from 77 to 92%; absolute proximal reabsorption rate of sodium remained constant. ANG II decreased sodium excretion by 70%, potassium excretion by 50%, and urine flow by 80%, whereas urine osmolality increased. ANG III also increased plasma aldosterone markedly (+45%), however, without measurable changes in angiotensin immunoreactivity, glomerular filtration rate, or renal excretion rates. During vehicle infusion, plasma renin activity decreased markedly (∼700 to ∼200 mIU/l); only ANG II enhanced this decrease. ANG-(1-7) and ANG IV did not change any of the measured variables persistently. It is concluded that 1) ANG III and ANG IV are cleared much faster from plasma than ANG II, 2) ANG II causes hypofiltration, urinary concentration, and sodium and potassium retention at constant plasma concentrations of vasopressin and atrial natriuretic peptide, and 3) a very small increase in the concentration of ANG III, undetectable by usual techniques, may increase aldosterone secretion substantially.
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Ling, Shuang, Ju Duan, Rongzhen Ni, and Jin-Wen Xu. "2,3,5,4′-Tetrahydroxystilbene-2-O-β-D-glucoside Promotes Expression of the Longevity Gene Klotho." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/3128235.
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The longevity gene klotho has numerous physiological functions, such as regulating calcium and phosphorus levels, delaying senescence, improving cognition, reducing oxidative stress, and protecting vascular endothelial cells. This study tested whether 2,3,5,4′-Tetrahydroxystilbene-2-O-β-D-glucoside (THSG), a small molecule with antiaging effects, regulates the expression and physiological effects of klotho. Our results showed that THSG dose-dependently increased the luciferase reporter activity of the klotho gene, reversed the decrease in mRNA and protein expression of klotho which was induced by angiotensin II in NRK-52E renal tubular epithelial cells, and increased klotho mRNA expression in the cerebral cortex, hippocampus, testis, and kidney medulla of spontaneously hypertensive rats. THSG also reduced the number of senescent cells induced by angiotensin II and improved the antioxidant capacity and enhanced the bone strength in vivo. Based on klotho’s role in promoting cognition, regulating bone metabolism, and improving renal function, the effect of THSG on klotho expression will be beneficial to the functional improvement or enhancement of the expressed organs or tissues.
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Pevtsova, E. I., S. M. Tolpygo, M. F. Obukhova, and A. V. Kotov. "Physiological effects of complexes of angiotensins with functionally different carrier proteins." Bulletin of Experimental Biology and Medicine 146, no. 2 (August 2008): 172–75. http://dx.doi.org/10.1007/s10517-008-0240-1.
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Torsoni, MA, JB Carvalheira, VC Calegari, RM Bezerra, MJ Saad, JA Gontijo, and LA Velloso. "Angiotensin II (AngII) induces the expression of suppressor of cytokine signaling (SOCS)-3 in rat hypothalamus - a mechanism for desensitization of AngII signaling." Journal of Endocrinology 181, no. 1 (April 1, 2004): 117–28. http://dx.doi.org/10.1677/joe.0.1810117.
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Angiotensin II exerts a potent dypsogenic stimulus on the hypothalamus, which contributes to its centrally mediated participation in the control of water balance and blood pressure. Repetitive intracerebroventricular (i.c.v.) injections of angiotensin II lead to a loss of effect characterized as physiological desensitization to the peptide's action. In the present study, we demonstrate that angiotensin II induces the expression of suppressor of cytokine signaling (SOCS)-3 via angiotensin receptor 1 (AT1) and JAK-2, mostly located at the median preoptic lateral and anterodorsal preoptic nuclei. SOCS-3 produces an inhibitory effect upon the signal transduction pathways of several cytokines and hormones that employ members of the JAK/STAT families as intermediaries. The partial inhibition of SOCS-3 translation by antisense oligonucleotide was sufficient to significantly reduce the refractoriness of repetitive i.c.v. angiotensin II injections, as evaluated by water ingestion. Thus, by acting through AT1 on the hypothalamus, angiotensin II induces the expression of SOCS-3 which, in turn, blocks further activation of the pathway and consequently leads to desensitization to angiotensin II stimuli concerning its dypsogenic effect.
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Pashova-Stoyanova, L., and A. Tolekova. "Effects of vitamin D on the renin-angiotensin system." Trakia Journal of Sciences 17, no. 3 (2019): 277–82. http://dx.doi.org/10.15547/tjs.2019.03.017.
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The renin-angiotensin-aldosterone system (RAAS) is a complex endocrine system of enzymes, proteins and peptides that occupies a key position in the regulation of a number of important physiological processes, such as arterial pressure, water and electrolyte homeostasis. Its activity, flow and regulation are affected by a large number of mediators, substances and diseases one of which is vitamin D. Vitamin D is involved in the regulation of many physiological processes with great importance. Vitamin D deficiency is associated with an increased risk of impaired renal function, cardiovascular disease, diabetes mellitus, metabolic disorders, affecting RAAS and other pathways
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Csikós, Tamás, Stefan Gallinat, and Thomas Unger. "Extrarenal aspects of angiotensin II function." European Journal of Endocrinology 136, no. 4 (April 1997): 349–58. http://dx.doi.org/10.1530/eje.0.1360349.
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Abstract The cloning of angiotensin II (Ang II) receptor genes and the availability of specific receptor ligands allows characterization of Ang II receptor-mediated actions. Most of the well-known Ang II effects such as vasoconstriction, drinking response and cell proliferation are mediated through the AT1 receptor. Little is known about the physiological effect of the AT2 receptor, though there are some reports describing the involvement of the AT2 receptor in blood pressure regulation. Recent data demonstrate that the AT2-mediated actions are inhibitory to AT1- and mitogen-induced growth effects, indicating a balancing mechanism for Ang II-controlled mechanisms. It has also been demonstrated that AT2 receptor inactivation induces endothelial cell proliferation in the presence of Ang II. Additionally, AT2 receptor activation enhances nerve growth factor-induced differentiation of PC12W cells and a role in apoptotic changes has also been reported. Based on recent findings, this article focuses on the role of Ang II in growth and differentiation processes with respect to the AT2 receptor in these events. European Journal of Endocrinology 136 349–358
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RICKETTS, Marie L., and Paul M. STEWART. "Regulation of 11β-hydroxysteroid dehydrogenase type 2 by diuretics and the renin–angiotensin–aldosterone axis." Clinical Science 96, no. 6 (May 12, 1999): 669–75. http://dx.doi.org/10.1042/cs0960669.
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In the kidney and colon 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) inactivates cortisol to cortisone, thereby protecting the non-selective mineralocorticoid receptor from cortisol. Deficiency of 11β-HSD2 results in cortisol-mediated sodium retention and hypertension, suggesting that the physiological regulation of 11β-HSD2 in mineralocorticoid target tissues may be important in modulating sodium homoeostasis and blood pressure control. Using the human epithelial colon cell line SW-620, reverse transcriptase-polymerase chain reaction and enzyme kinetic analysis indicated expression of only 11β-HSD2 (Km for cortisol 66 nmol/l). Bradykinin (10-8 to 10-12 mol/l), frusemide (10-4 to 10-9 mol/l), benzamiloride hydrochloride (10-5 to 10-10 mol/l) and atrial natriuretic peptide (10-6 to 10-10 mol/l) had no effect on 11β-HSD2 expression. Using a range of concentrations of angiotensin II (2×10-8 to 2×10-5 mol/l) a significant reduction in activity was seen but only at supra-physiological concentrations, [e.g. 2×10-6 mol/l at 4 h pretreatment: 36.7±2.0 pmol cortisone·h-1·mg-1 (mean±S.E.M.) compared with 45.1±1.7 pmol·h-1·mg-1 in control; P < 0.05]. The angiotensin-converting enzyme inhibitors captopril, enalapril, lisinopril, perindopril, quinapril and trandolapril at 10-7 mol/l, but not fosinopril, significantly increased 11β-HSD2 activity after pretreatment for 16 or 24 h (P < 0.05-P < 0.01 compared with control). No effects were seen at 4 h pretreatment. Hydrochlorothiazide (10-7 mol/l) significantly decreased 11β-HSD2 activity (P < 0.05 compared with control) at 4 h pretreatment. Commonly used diuretics, atrial natriuretic peptide and physiological concentrations of angiotensin II and bradykinin do not alter 11β-HSD2 activity. In contrast, a series of angiotensin-converting enzyme inhibitors significantly increase 11β-HSD2 activity in vitro. This may explain how intrarenal infusions of angiotensin-converting enzyme inhibitors increase renal sodium excretion independent of circulating concentrations of angiotensin II. The interaction between angiotensin-converting enzyme inhibitors and 11β-HSD2 may be an additional mechanism by which the former can lower blood pressure.
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Bruun, N. E., P. Skott, and J. Giese. "Renal and endocrine effects of physiological variations of atrial natriuretic factor in normal humans." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 260, no. 1 (January 1, 1991): R217—R224. http://dx.doi.org/10.1152/ajpregu.1991.260.1.r217.
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The renal and endocrine effects of incremental infusions of 3 and 6 ng.kg-1.min-1 of exogenous atrial natriuretic factor (ANF)-(99-126) or placebo were investigated in 10 normal subjects. A 90-min basal period was followed by two 2-h infusion periods with urine collection in the last 90 min of each period. Plasma ANF concentration increased by 50 and 150%, respectively, from a basal value of 6.2 +/- 3.1 pmol/l. Plasma guanosine 3',5'-cyclic monophosphate concentration increased in parallel with ANF. Blood pressure and heart rate were unchanged, whereas hematocrit was stepwise increased. 51Cr-EDTA clearance (GFR) did not change, but ANF caused an increase in Li clearance (a measure of end-proximal fluid delivery), Na clearance, and urine flow compared with time-matched control values. These excretory effects of ANF were mainly due to prevention of the 20- to 50% decreases occurring in the placebo series. Calculated values of fractional proximal and distal tubular Na reabsorption decreased significantly. ANF caused a decrease in plasma concentrations of active renin and aldosterone, whereas renin substrate, angiotensin I, and angiotensin II concentrations were unaltered. A subtle increase in plasma concentrations of norepinephrine and epinephrine was observed during the ANF infusions. These data suggest that the natriuretic effect of ANF is caused by an increased fluid delivery from the proximal tubule in addition to a fall in fractional distal Na reabsorption.
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Herr, D., M. Rodewald, H. M. Fraser, G. Hack, R. Konrad, R. Kreienberg, and C. Wulff. "Regulation of endothelial proliferation by the renin–angiotensin system in human umbilical vein endothelial cells." REPRODUCTION 136, no. 1 (July 2008): 125–30. http://dx.doi.org/10.1530/rep-07-0374.
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This study was performed in order to evaluate the role of angiotensin II in physiological angiogenesis. Human umbilical vein endothelial cells (HUVEC) were stained for angiotensin II type 1 receptor (AGTR1) immunocytochemically and for gene expression of renin–angiotensin system (RAS) components. The regulation of the angiogenesis-associated genes vascular endothelial growth factor (VEGF) and angiopoietins (ANGPT1andANGPT2) were studied using quantitative RT-PCR. Furthermore, we examined the effect of angiotensin II on the proliferation of HUVEC using Ki-67 as well as BrdU immunocytochemistry and investigated whether the administration of the AGTR1 blocker candesartan or the VEGF antagonist FLT1-Fc could suppress the observed angiotensin II-dependent proangiogenic effect. AGTR1 was expressed in HUVEC and the administration of angiotensin II significantly increased the gene expression ofVEGFand decreased the gene expression ofANGPT1. Since the expression ofANGPT2was not affected significantly the ratio of ANGPT1/ANGPT2 was decreased. In addition, a significantly increased endothelial cell proliferation was observed after stimulation with angiotensin II, which was suppressed by the simultaneous administration of candesartan or the VEGF antagonist FLT1-Fc. These results indicate the potential capacity of angiotensin II in influencing angiogenesis by the regulation of angiogenesis-associated genes via AGTR1. Since VEGF blockade opposed the effect of angiotensin II on cell proliferation, it is hypothesised that VEGF mediates the angiotensin II-dependent effect in concert with the changes in angiopoietin expression. This is the first report of the RAS on the regulation of angiogenesis-associated genes in physiology.
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Charles, Christopher J., Miriam T. Rademaker, and A. Mark Richards. "Urocortin 1 modulates the neurohumoral response to acute nitroprusside-induced hypotension in sheep." Clinical Science 112, no. 9 (April 2, 2007): 485–91. http://dx.doi.org/10.1042/cs20060303.
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In addition to haemodynamic actions, Ucn1 (urocortin 1) has been reported to affect a number of hormonal systems; however, it remains unclear whether Ucn1 modulates circulating hormones under physiological conditions. Accordingly, in the present study, we have examined the effects of Ucn1 on haemodynamics, hormones and renal indices in normal conscious sheep subjected to a nitroprusside-induced hypotensive stimulus designed to alter hormonal levels within the physiological range. Ucn1 administration did not alter the haemodynamic response to nitroprusside-induced hypotension. However, compared with the rise observed on the control day, plasma ANP (atrial natriuretic peptide; P=0.043), BNP (brain natriuretic peptide; P=0.038) and endothelin-1 (P=0.011) levels were reduced following Ucn1 administration. Associated with this significant reduction in natriuretic peptides, the increase in urinary sodium output associated with rising pressures post-nitroprusside was abolished following Ucn1 administration (P=0.048). Ucn1 had no significant effect on the response of hormones of the renin–angiotensin–aldosterone system or the hypothalamo–pituitary–adrenal axis. In conclusion, Ucn1, administered at physiologically relevant levels during nitroprusside-induced hypotension, attenuates the secretion/release of endothelin-1 and the cardiac natriuretic peptides ANP and BNP. Suppression of ANP and BNP probably led to an attenuated natriuretic response to recovery from acute hypotension. The threshold for the action of Ucn1 on the natriuretic peptides and endothelin-1 appears to be below that of other actions of Ucn1.
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Kojima, I., H. Shibata, and E. Ogata. "Phorbol ester inhibits angiotensin-induced activation of phospholipase C in adrenal glomerulosa cells. Its implication in the sustained action of angiotensin." Biochemical Journal 237, no. 1 (July 1, 1986): 253–58. http://dx.doi.org/10.1042/bj2370253.
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The present study was undertaken to determine whether an agonist-induced activation of C-kinase leads to an inhibition of phospholipase C in adrenal glomerulosa cells. When cells are treated with 100 nM-TPA (12-O-tetradecanoylphorbol 13-acetate), subsequent angiotensin (‘angiotensin II’)-induced aldosterone secretion is greatly inhibited. Treatment with TPA completely inhibits the angiotensin-induced increase in both inositol trisphosphate and the cytosolic Ca2+ concentration. The dose-response curve for TPA-induced inhibition reveals that quite a high concentration of TPA is necessary to block angiotensin action compared with that needed to stimulate aldosterone secretion. 1-Oleoyl-2-acetylglycerol has a weak inhibitory effect, whereas neither 4 alpha-phorbol 12,13-didecanoate or 4 beta-phorbol inhibits angiotensin action. When the time course of changes in inositol trisphosphate and diacylglycerol is measured, angiotensin action is sustained for up to 30 min. In addition, 100 nM-TPA added after 20 min of angiotensin addition attenuates production of both inositol trisphosphate and diacylglycerol. These results suggest that high dose of TPA inhibits angiotensin-induced activation of phospholipase C by acting, at least partly, on C-kinase, but that an inhibitory effect of TPA may be a pharmacological effect with little physiological significance in this system.
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Schmaier, Alvin H. "The kallikrein-kinin and the renin-angiotensin systems have a multilayered interaction." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 285, no. 1 (July 2003): R1—R13. http://dx.doi.org/10.1152/ajpregu.00535.2002.
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Understanding the physiological role of the plasma kallikrein-kinin system (KKS) has been hampered by not knowing how the proteins of this proteolytic system, when assembled in the intravascular compartment, become activated under physiological conditions. Recent studies indicate that the enzyme prolylcarboxypeptidase, an ANG II inactivating enzyme, is a prekallikrein activator. The ability of prolylcarboxypeptidase to act in the KKS and the renin-angiotensin system (RAS) indicates a novel interaction between these two systems. This interaction, along with the roles of angiotensin converting enzyme, cross talk between bradykinin and angiotensin-( 1 – 7 ) action, and the opposite effects of activation of the ANG II receptors 1 and 2 support a hypothesis that the plasma KKS counterbalances the RAS. This review examines the interaction and cross talk between these two protein systems. This analysis suggests that there is a multilayered interaction between these two systems that are important for a wide array of physiological functions.
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Okunishi, Hideki, Kenji Ishii, Hiroshi Sakonjo, Yuko Oka, and Mizuo Miyazaki. "Hypotensive and diuretic effects of renin-angiotensin system (RAS) blockers; Physiological role of angiotensin II (AII)." Japanese Journal of Pharmacology 58 (1992): 68. http://dx.doi.org/10.1016/s0021-5198(19)48703-9.
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Jennings, Donald B. "Cardiorespiratory effects of prolonged angiotensin II block in resting conscious dogs." Canadian Journal of Physiology and Pharmacology 79, no. 9 (September 1, 2001): 825–30. http://dx.doi.org/10.1139/y01-057.
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Intravenous (iv) infusion of the angiotensin II (ANG II) receptor blocker saralasin in resting conscious dogs during physiological pertubations, such as hypotension and prolonged hypoxia, indicates the presence of an ANG II drive to increase respiration and decrease the arterial partial pressure of CO2 (PaCO2). In contrast, in eupneic resting dogs on a regular chow diet, iv infusion of saralasin for short periods (up to 30 min) provides no evidence of a tonic effect of circulating levels of ANG II on acid-base balance, respiration, metabolism, or circulation. However, ANG II influences physiological processes involving salt, water, and acid-base balances, which are potentially expressed beyond a 30 min time period, and could secondarily affect respiration. Therefore, we tested the hypothesis that blocking ANG II with iv saralasin would affect respiration and circulation over a 4-h period. Contrary to the hypothesis, iv infusion of saralasin in resting conscious eupneic dogs on a regular chow diet over a 4-h period had no effects on plasma strong ions, osmolality, acid-base balance, respiration, metabolism, or circulation when compared with similar control studies in the same animals. Thus, ANG II does not play a tonic modulatory role in respiratory control under "normal" physiological conditions.Key words: acid-base balance, arginine vasopressin, saralasin, strong ions, strong ion difference.
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Cano, A., R. T. Miller, R. J. Alpern, and P. A. Preisig. "Angiotensin II stimulation of Na-H antiporter activity is cAMP independent in OKP cells." American Journal of Physiology-Cell Physiology 266, no. 6 (June 1, 1994): C1603—C1608. http://dx.doi.org/10.1152/ajpcell.1994.266.6.c1603.
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Angiotensin II has been reported to stimulate the proximal tubule Na-H antiporter by inhibition of adenylyl cyclase, and possibly by an adenosine 3',5'-cyclic monophosphate (cAMP)-independent mechanism. We examined the effect of angiotensin II on Na-H antiporter activity (JNa-H) in opossum kidney (OKP) cells, a proximal tubule-like cell line, whose Na-H antiporter resembles that of the proximal tubule apical membrane. We found that angiotensin II regulates JNa-H in a concentration-dependent manner similar to the proximal tubule, with angiotensin II concentrations < 10(-8) M stimulating and > 10(-8) M inhibiting JNa-H. The stimulatory effect of angiotensin II was blocked by 10(-8) M losartan and was pertussis toxin sensitive, suggesting mediation through an angiotensin II (AT1) receptor coupled to a pertussis toxin-sensitive G protein. Acute treatment with 10(-4) M 8-bromoadenosine 3',5'-cyclic monophosphate (8-BrcAMP) inhibited JNa-H by 30% and blocked angiotensin II-induced stimulation. However, angiotensin II (10(-12)-10(-6) M) did not inhibit basal, dopamine-stimulated, or forskolin-stimulated cAMP production measured in the presence of 3-isobutyl-1-methylxanthine (IBMX). In addition, angiotensin II had no effect on cAMP levels measured in the absence of IBMX. We conclude that angiotensin II at physiological concentrations stimulates JNa-H in OKP cells via a cAMP-independent mechanism mediated by an AT1 receptor and a pertussis toxin-sensitive G protein.
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Paul, Martin, Ali Poyan Mehr, and Reinhold Kreutz. "Physiology of Local Renin-Angiotensin Systems." Physiological Reviews 86, no. 3 (July 2006): 747–803. http://dx.doi.org/10.1152/physrev.00036.2005.
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Since the first identification of renin by Tigerstedt and Bergmann in 1898, the renin-angiotensin system (RAS) has been extensively studied. The current view of the system is characterized by an increased complexity, as evidenced by the discovery of new functional components and pathways of the RAS. In recent years, the pathophysiological implications of the system have been the main focus of attention, and inhibitors of the RAS such as angiotensin-converting enzyme (ACE) inhibitors and angiotensin (ANG) II receptor blockers have become important clinical tools in the treatment of cardiovascular and renal diseases such as hypertension, heart failure, and diabetic nephropathy. Nevertheless, the tissue RAS also plays an important role in mediating diverse physiological functions. These focus not only on the classical actions of ANG on the cardiovascular system, namely, the maintenance of cardiovascular homeostasis, but also on other functions. Recently, the research efforts studying these noncardiovascular effects of the RAS have intensified, and a large body of data are now available to support the existence of numerous organ-based RAS exerting diverse physiological effects. ANG II has direct effects at the cellular level and can influence, for example, cell growth and differentiation, but also may play a role as a mediator of apoptosis. These universal paracrine and autocrine actions may be important in many organ systems and can mediate important physiological stimuli. Transgenic overexpression and knock-out strategies of RAS genes in animals have also shown a central functional role of the RAS in prenatal development. Taken together, these findings may become increasingly important in the study of organ physiology but also for a fresh look at the implications of these findings for organ pathophysiology.
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Caroccia, Brasilina, Teresa Maria Seccia, Maria Piazza, Selene Prisco, Sofia Zanin, Maurizio Iacobone, Livia Lenzini, et al. "Aldosterone Stimulates Its Biosynthesis Via a Novel GPER-Mediated Mechanism." Journal of Clinical Endocrinology & Metabolism 104, no. 12 (May 24, 2019): 6316–24. http://dx.doi.org/10.1210/jc.2019-00043.
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Abstract Context The G protein–coupled estrogen receptor (GPER) mediates an aldosterone secretagogue effect of 17β-estradiol in human HAC15 adrenocortical cells after estrogen receptor β blockade. Because GPER mediates mineralocorticoid receptor-independent aldosterone effects in other cell types, we hypothesized that aldosterone could modulate its own synthesis via GPER activation. Methods HAC15 cells were exposed to aldosterone in the presence or absence of canrenone, a mineralocorticoid receptor antagonist, and/or of the selective GPER antagonist G36. Aldosterone synthase (CYP11B2) mRNA and protein levels changes were the study end points. Similar experiments were repeated in strips obtained ex vivo from aldosterone-producing adenoma (APA) and in GPER-silenced HAC15 cells. Results Aldosterone markedly increased CYP11B2 mRNA and protein expression (vs untreated samples, P < 0.001) in both models by acting via GPER, because these effects were abolished by G36 (P < 0.01) and not by canrenone. GPER-silencing (P < 0.01) abolished the aldosterone-induced increase of CYP11B2, thus proving that aldosterone acts via GPER to augment the step-limiting mitochondrial enzyme (CYP11B2) of its synthesis. Angiotensin II potentiated the GPER-mediated effect of aldosterone on CYP11B2. Coimmunoprecipitation studies provided evidence for GPER-angiotensin type-1 receptor heterodimerization. Conclusion We propose that this autocrine-paracrine mechanism could enhance aldosterone biosynthesis under conditions of immediate physiological need in which the renin-angiotensin-aldosterone system is stimulated as, for example, hypovolemia. Moreover, as APA overexpresses GPER this mechanism could contribute to the aldosterone excess that occurs in primary aldosteronism in a seemingly autonomous fashion from angiotensin II.
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Dibona, G. F., S. Y. Jones, and L. L. Sawin. "Effect of endogenous angiotensin II on renal nerve activity and its cardiac baroreflex regulation." Journal of the American Society of Nephrology 9, no. 11 (November 1998): 1983–89. http://dx.doi.org/10.1681/asn.v9111983.
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The effects of physiologic alterations in endogenous angiotensin II activity on basal renal sympathetic nerve activity and its cardiac baroreflex regulation were studied. The effect of angiotensin II type 1 receptor blockade with intracerebroventricular losartan was examined in conscious rats consuming a low, normal, or high sodium diet that were instrumented for the simultaneous measurement of right atrial pressure and renal sympathetic nerve activity. The gain of cardiac baroreflex regulation of renal sympathetic nerve activity (% delta renal sympathetic nerve activity/mmHg mean right atrial pressure) was measured during isotonic saline volume loading. Intracerebroventricular losartan did not decrease arterial pressure but significantly decreased renal sympathetic nerve activity in low (-36+/-6%) and normal (-24+/-5%), but not in high (-2+/-3%) sodium diet rats. Compared with vehicle treatment, losartan treatment significantly increased cardiac baroreflex gain in low (-3.45+/-0.20 versus -2.89+/-0.17) and normal (-2.89+/-0.18 versus -2.54+/-0.14), but not in high (-2.27+/-0.15 versus -2.22+/-0.14) sodium diet rats. These results indicate that physiologic alterations in endogenous angiotensin II activity tonically influence basal levels of renal sympathetic nerve activity and its cardiac baroreflex regulation.
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Brown, J. Anne, Richard K. Paley, Shehla Amer, and Stephen J. Aves. "Evidence for an intrarenal renin-angiotensin system in the rainbow trout, Oncorhynchus mykiss." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 278, no. 6 (June 1, 2000): R1685—R1691. http://dx.doi.org/10.1152/ajpregu.2000.278.6.r1685.
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Physiological and molecular approaches were used to investigate the existence of an intrarenal renin-angiotensin system (RAS) in rainbow trout. Inhibition of angiotensin-converting enzyme by captopril (5 × 10− 4 M) rapidly decreased vascular resistance of the trunk of the trout, perfused at 19 mmHg, resulting in an increased perfusate flow rate and a decreased intrarenal dorsal aortic pressure. A profound diuresis occurred in the in situ perfused kidney and reflected both increased glomerular filtration rates and decreased water reabsorption (osmolyte reabsorption was unchanged). Renal and vascular parameters recovered once captopril treatment was stopped. Diuretic and vascular effects of captopril on the in situ trout kidney concur with an inhibition of known vasoconstrictor and antidiuretic actions of angiotensin II. However, at a higher perfusion pressure (28 mmHg), captopril had no effect on intrarenal aortic pressure or perfusate and urine flow rates, suggesting that the trout intrarenal RAS is activated by low perfusion pressures/flows. Existence of the renal RAS in trout was further supported by evidence for angiotensinogen gene expression in kidney as well as liver.
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Seidelin, Peter H., John J. McMurray, and Allan D. Struthers. "Mechanisms of the antinatriuretic action of physiological doses of angiotensin II in man." Clinical Science 76, no. 6 (June 1, 1989): 653–58. http://dx.doi.org/10.1042/cs0760653.
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1. Angiotensin 11 (ANG II; 1 ng min−1 kg−1) or 5% (w/v) d-glucose (placebo) was infused in six normal male volunteers, pretreated with 500 mg of lithium carbonate, who were undergoing maximal water diuresis. 2. This dose of ANG II caused a circulating increment within the physiological range (27 ± 4 to 48 ± 9 pmol/l). 3. Compared with placebo, ANG II caused a significant fall in urinary sodium excretion (113 ± 13 to 82 ± 10 μmol/min). This antinatriuretic effect occurred without a fall in creatinine clearance (107 ± 3 versus 113 ± 3 ml/min). 4. ANG II caused a significant fall in fractional lithium clearance (28 ± 2 to 23 ± 2%). This may indicate a proximal tubular effect of ANG II. 5. ANG II also reduced fractional distal delivery [(sodium clearance plus free water clearance) divided by creatinine clearance], another measure of proximal tubular outflow. A parallel change in these two separate markers of proximal function supports an action of ANG II at this nephron segment. 6. Furthermore, the antinatriuretic effect of ANG II was unlikely to be due to stimulation of aldosterone secretion because (a) the fall in sodium excretion was temporally dissociated from the rise in aldosterone secretion, (b) potassium excretion also tended to fall during ANG II infusion and (c) aldosterone has a distal nephron effect, while, in this study, proximal nephron fractional reabsorption of sodium increased and distal nephron fractional reabsorption of sodium was unchanged. 7. These observations suggest that physiological increments in ANG II can have an antinatriuretic effect in man, which, at least initially, results from increased proximal tubular sodium reabsorption and is independent of the effect of aldosterone.
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Mattiazzi, A., N. G. Perez, M. G. Vila-Petroff, B. Alvarez, M. C. Camilion de Hurtado, and H. E. Cingolani. "Dissociation between positive inotropic and alkalinizing effects of angiotensin II in feline myocardium." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 3 (March 1, 1997): H1131—H1136. http://dx.doi.org/10.1152/ajpheart.1997.272.3.h1131.
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The present study examines the intracellular pH (pHi) dependence of angiotensin (ANG) II-induced positive inotropic effect in cat papillary muscles contracting isometrically (0.2 Hz, 30 degrees C). Muscles were loaded with the fluorescent dye 2'-7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein acetoxymethyl ester for simultaneous measurement of pHi and contractility. In N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES) buffer (n = 4), there was a temporal dissociation between the positive inotropic and the alkalinizing effects of ANG II (0.5 microM). The positive inotropic effect of ANG II peaked at 9.7 +/- 0.8 min (240 +/- 57% above control) without significant changes in pHi. The increase in pHi became significant (0.05 +/- 0.01 pH units) only after 16 min of exposure to the drug, when the positive inotropic effect of ANG II was already fading. In HCO3- buffer (n = 7), the ANG II-induced positive inotropic effect occurred without significant pHi changes. In the presence of 5 microM ethyl isopropyl amiloride (EIPA, to specifically inhibit the Na+/H+ exchanger), the alkalinizing effect of ANG II was changed to a significant decrease in pHi, despite which ANG II still increased contractility by 87 +/- 16% (n = 6). The results indicate that in HEPES buffer only a fraction of the ANG II-induced positive inotropic effect can be attributed to a pHi change, whereas in a physiological CO2-HCO3- medium the positive inotropic effect of ANG II is independent of pHi changes. Furthermore, an ANG II-induced increase in myocardial contractility was observed even when ANG II administration elicited a decrease in pHi, as occurred after Na+/H+ exchanger blockade. The results show that in feline myocardium, the increase in contractility evoked by ANG II in a physiological CO2-HCO3- medium is not due to an increase in Ca2+ myofilament sensitivity secondary to an increase in myocardial pHi.
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Satoh, Nobuhiko, Motonobu Nakamura, Atsushi Suzuki, Hiroyuki Tsukada, Shoko Horita, Masashi Suzuki, Kyoji Moriya, and George Seki. "Effects of Nitric Oxide on Renal Proximal Tubular Na+Transport." BioMed Research International 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/6871081.
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Nitric oxide (NO) has a wide variety of physiological functions in the kidney. Besides the regulatory effects in intrarenal haemodynamics and glomerular microcirculation,in vivostudies reported the diuretic and natriuretic effects of NO. However, opposite results showing the stimulatory effect of NO on Na+reabsorption in the proximal tubule led to an intense debate on its physiological roles. Animal studies have showed the biphasic effect of angiotensin II (Ang II) and the overall inhibitory effect of NO on the activity of proximal tubular Na+transporters, the apical Na+/H+exchanger isoform 3, basolateral Na+/K+ATPase, and the Na+/HCO3-cotransporter. However, whether these effects could be reproduced in humans remained unclear. Notably, our recent functional analysis of isolated proximal tubules demonstrated that Ang II dose-dependently stimulated human proximal tubular Na+transport through the NO/guanosine 3′,5′-cyclic monophosphate (cGMP) pathway, confirming the human-specific regulation of proximal tubular transport via NO and Ang II. Of particular importance for this newly identified pathway is its possibility of being a human-specific therapeutic target for hypertension. In this review, we focus on NO-mediated regulation of proximal tubular Na+transport, with emphasis on the interaction with individual Na+transporters and the crosstalk with Ang II signalling.
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Garcia-Garrote, Maria, Juan A. Parga, Pablo J. Labandeira, Jose Luis Labandeira-Garcia, and Jannette Rodriguez-Pallares. "Dopamine Regulates Adult Neurogenesis in the Ventricular-Subventricular Zone via Dopamine D3 Angiotensin Type 2 Receptor Interactions." Stem Cells 39, no. 12 (September 20, 2021): 1778–94. http://dx.doi.org/10.1002/stem.3457.
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Abstract Adult neurogenesis is a dynamic and highly regulated process, and different studies suggest that dopamine modulates ventricular-subventricular zone (V-SVZ) neurogenesis. However, the specific role of dopamine and the mechanisms/factors underlying its effects on physiological and pathological conditions such as Parkinson's disease (PD) are not fully understood. Recent studies have described counter-regulatory interactions between renin-angiotensin system (RAS) and dopamine in peripheral tissues and in the nigrostriatal system. We have previously demonstrated that angiotensin receptors regulate proliferation and generation of neuroblasts in the rodent V-SVZ. However, possible interactions between dopamine receptors and RAS in the V-SVZ and their role in alterations of neurogenesis in animal models of PD have not been investigated. In V-SVZ cultures, activation of dopamine receptors induced changes in the expression of angiotensin receptors. Moreover, dopamine, via D2-like receptors and particularly D3 receptors, increased generation of neurospheres derived from the V-SVZ and this effect was mediated by angiotensin type-2 (AT2) receptors. In rats, we observed a marked reduction in proliferation and generation of neuroblasts in the V-SVZ of dopamine-depleted animals, and inhibition of AT1 receptors or activation of AT2 receptors restored proliferation and generation of neuroblasts to control levels. Moreover, intrastriatal mesencephalic grafts partially restored proliferation and generation of neuroblasts observed in the V-SVZ of dopamine-depleted rats. Our data revealed that dopamine and angiotensin receptor interactions play a major role in the regulation of V-SVZ and suggest potential beneficial effects of RAS modulators on the regulation of adult V-SVZ neurogenesis.
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Tuchelt, H., G. Eschenhagen, V. Bähr, G. Schwietzer, H. M. Thiede, and W. Oelkers. "Role of Atrial Natriuretic Factor in Changes in the Responsiveness of Aldosterone to Angiotensin II Secondary to Sodium Loading and Depletion in Man." Clinical Science 79, no. 1 (July 1, 1990): 57–65. http://dx.doi.org/10.1042/cs0790057.
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1. Sodium loading blunts the response of aldosterone to infusion of angiotensin II, whereas sodium depletion leads to an enhanced response. The hypothesis was tested that these changes in responsiveness of the zona glomerulosa are mediated in part by changes in plasma atrial natriuretic factor levels. 2. To this end, plasma renin activity and plasma aldosterone were measured in the upright and recumbent position and during incremental infusions of angiotensin II (1, 3 and 6 ng of angiotensin II amide min−1 kg−1 for 1 h each dose) after 6 days of sodium loading (study 1), after 5 days of sodium depletion (study 2) and after sodium depletion plus infusion of atrial natriuretic factor (0.13 μg/min for 8 h) on the test day (study 3). Six normal young males were investigated. 3. Plasma atrial natriuretic factor levels were around 5 pmol/l in study 2, 15 pmol/l in study 1 and 15 pmol/l in study 3 during infusion of atrial natriuretic factor. Two hours after the onset of atrial natriuretic factor infusion, plasma renin activity and plasma aldosterone (recumbent) were markedly and significantly lower in study 3 than in study 2, but still significantly higher than in study 1. The increase in plasma aldosterone after infusion of angiotensin II was slightly, but not significantly, blunted by infusion of atrial natriuretic factor in study 3 compared with study 2. The overall increase in plasma aldosterone was still significantly greater in study 3 than in study 1. 4. The fall in renal plasma flow, determined as p-aminohippurate clearance, during infusion of angiotensin II was greater in study 1 than in studies 2 and 3. Small differences between study 3 and study 2 were not significant. 5. It is concluded that infusions of atrial natriuretic factor in the low-sodium state that mimic plasma atrial natriuretic factor levels after sodium loading lead to a marked fall in recumbent plasma aldosterone, which is to a large extent secondary to a fall in plasma renin activity. A small direct effect of these physiologically elevated atrial natriuretic factor levels on the zona glomerulosa itself (the increase in plasma aldosterone during angiotensin II infusion) was only of borderline significance. Thus, atrial natriuretic factor at physiological plasma concentrations is a regulator of renin and aldosterone secretion, whereas a modulating effect on the renal vasoconstrictor action of angiotensin II could not be demonstrated.
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Lawrence, D. L., J. B. Skatrud, and Y. Shenker. "Effect of hypoxia on atrial natriuretic factor and aldosterone regulation in humans." American Journal of Physiology-Endocrinology and Metabolism 258, no. 2 (February 1, 1990): E243—E248. http://dx.doi.org/10.1152/ajpendo.1990.258.2.e243.
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To evaluate the possible physiological role of atrial natriuretic factor (ANF) on the observed dissociation of aldosterone from the renin-angiotensin system during acute hypoxia, 7 men, ages 18-27 yr, were studied on two separate days for 1 h under hypoxic (12% O2) and normoxic (room air) conditions. Subjects were on a low-salt diet (urinary sodium 67 +/- 13 meq/24 h) and suppressed with dexamethasone. Hemoglobin saturation decreased during hypoxemia to 68 +/- 1% (P less than 0.01), whereas heart rate increased from 65 +/- 3 to 89 +/- 5 beats/min (P less than 0.01). Plasma aldosterone levels decreased 43% from basal during hypoxemia (P less than 0.01), whereas ANF levels increased by 50% (P less than 0.05). Levels of both were unchanged during normoxemia. Plasma renin activity, angiotensin II, blood pressure, and pH did not change under either condition, and plasma cortisol levels were totally suppressed. These results indicate that acute hypoxemia is a potent stimulus for ANF release and that ANF is probably a major factor responsible for the dissociation of aldosterone from the renin-angiotensin system under these conditions.
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Fletcher, Eugene C. "Invited Review: Physiological consequences of intermittent hypoxia: systemic blood pressure." Journal of Applied Physiology 90, no. 4 (April 1, 2001): 1600–1605. http://dx.doi.org/10.1152/jappl.2001.90.4.1600.
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One of the major manifestations of obstructive sleep apnea is profound and repeated hypoxia during sleep. Acute hypoxia leads to stimulation of the peripheral chemoreceptors, which in turn increases sympathetic outflow, acutely increasing blood pressure. The chronic effect of these repeated episodic or intermittent periods of hypoxia in humans is difficult to study because chronic cardiovascular changes may take many years to manifest. Rodents have been a tremendous source of information in short- and long-term studies of hypertension and other cardiovascular diseases. Recurrent short cycles of normoxia-hypoxia, when administered to rats for 35 days, allows examination of the chronic cardiovascular response to intermittent hypoxia patterned after the episodic desaturation seen in humans with sleep apnea. The result of this type of intermittent hypoxia in rats is a 10- to 14-mmHg increase in resting (unstimulated) mean blood pressure that lasts for several weeks after cessation of the daily cyclic hypoxia. Carotid body denervation, sympathetic nerve ablation, renal sympathectomy, adrenal medullectomy, and angiotensin II receptor blockade block the blood pressure increase. It appears that adrenergic and renin-angiotensin system overactivity contributes to the early chronic elevated blood pressure in rat intermittent hypoxia and perhaps to human hypertension associated with obstructive sleep apnea.
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Tordoff, M. G., D. M. Pilchak, and R. L. Hughes. "Independence of salt intake induced by calcium deprivation from the renin-angiotensin-aldosterone system." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 264, no. 3 (March 1, 1993): R492—R499. http://dx.doi.org/10.1152/ajpregu.1993.264.3.r492.
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We investigated whether the elevated NaCl intake shown by calcium-deprived rats is mediated by the renin-angiotensin-aldosterone system. First, we looked for manifestations of altered renin-angiotensin-aldosterone system activity during the progression of calcium deficiency. There were no differences between control and calcium-deprived rats in plasma aldosterone concentrations, plasma renin activity, plasma sodium concentrations, sodium balance, or blood pressure. Second, we used selective pharmacological antagonists to examine whether disruption of the renin-aldosterone-angiotensin system influenced salt intake. Blockade of aldosterone receptors with spironolactone (25 mg.kg-1 x day-1 sc for 7 days) had no effect on NaCl intake of control or calcium-deprived rats. Angiotensin AT1 receptor blockade with losartan potassium (0.5-10 mg/kg orally) had no effect on NaCl intake of control or calcium-deprived rats but doses > 0.5 mg/kg decreased NaCl intake of adrenalectomized rats. Taken together, these findings indicate that the renin-angiotensin-aldosterone system does not mediate the increased NaCl intake produced by calcium deficiency. The appetite for salt produced by calcium deficiency involves a different physiological substrate from most other models of NaCl intake.
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Clark, Michelle A., Chinh Nguyen, and Hieu Tran. "Distinct Molecular Effects of Angiotensin II and Angiotensin III in Rat Astrocytes." International Journal of Hypertension 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/782861.
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It is postulated that central effects of angiotensin (Ang) II may be indirect due to rapid conversion to Ang III by aminopeptidase A (APA). Previously, we showed that Ang II and Ang III induced mitogen-activated protein (MAP) kinases ERK1/2 and stress-activated protein kinase/Jun-terminal kinases (SAPK/JNK) phosphorylation in cultured rat astrocytes. Most importantly, both peptides were equipotent in causing phosphorylation of these MAP kinases. In these studies, we used brainstem and cerebellum astrocytes to determine whether Ang II’s phosphorylation of these MAP kinases is due to the conversion of the peptide to Ang III. We pretreated astrocytes with 10 μM amastatin A or 100 μM glutamate phosphonate, selective APA inhibitors, prior to stimulating with either Ang II or Ang III. Both peptides were equipotent in stimulating ERK1/2 and SAPK/JNK phosphorylation. The APA inhibitors failed to prevent Ang II- and Ang III-mediated phosphorylation of the MAP kinases. Further, pretreatment of astrocytes with the APA inhibitors did not affect Ang II- or Ang III-induced astrocyte growth. These findings suggest that both peptides directly induce phosphorylation of these MAP kinases as well as induce astrocyte growth. These studies establish both peptides as biologically active with similar intracellular and physiological effects.