Role of kinins and angiotensin II in the renal hemodynamic response to captopril

1991 ◽  
Vol 260 (5) ◽  
pp. F670-F679 ◽  
Author(s):  
D. L. Mattson ◽  
R. J. Roman
Keyword(s):  
Angiotensin Ii ◽  
Wistar Rats ◽  
Plasma Renin ◽  
Hemodynamic Response ◽  
Ang Ii ◽  
Peritubular Capillary ◽  
Renal Hemodynamic ◽  
Vasa Recta ◽  
Capillary Pressures

This study examined the role of angiotensin II (ANG II), kinins, and prostaglandins in the renal hemodynamic response to captopril in Munich-Wistar rats in which plasma renin activity was elevated [18.8 +/- 3.3 ng angiotensin I (ANG I).ml-1.h-1]. Neural influences on the kidney were eliminated by renal denervation, and renal perfusion pressure (RPP) was controlled using a clamp on the aorta. Urine flow, sodium excretion, renal blood flow (RBF), glomerular filtration rate (GFR), and cortical and papillary red blood cell (RBC) flow increased significantly after captopril (2 mg/kg iv). Glomerular and peritubular capillary pressures rose by 20%, and vasa recta capillary pressure fell by 3-4 mmHg due to significant reductions in estimated preglomerular, efferent arteriolar and renal capillary-venous vascular resistances. Infusion of ANG II (20 ng.kg-1.min-1 iv) returned RBF, GFR, and glomerular and peritubular capillary pressures to control; however, ANG II did not lower papillary RBC flow before inhibition of prostaglandin synthesis. Saralasin had no effect on papillary RBC flow or the response to captopril. The changes in vasa recta hemodynamics produced by captopril were blocked by a kinin antagonist. These findings indicate that ANG II exerts a vasoconstrictor influence on the renal cortical vasculature of Munich-Wistar rats; however, its effects on the medullary circulation are opposed by vasodilatory eicosanoids. They also suggest that kinins participate in the papillary RBC flow response to captopril, perhaps by reducing the outflow resistance from the vasa recta circulation.

Control of descending vasa recta pericyte membrane potential by angiotensin II

2002 ◽  
Vol 282 (6) ◽  
pp. F1064-F1074 ◽  
Author(s):  
Thomas L. Pallone ◽  
James M.-C. Huang
Keyword(s):  
Membrane Potential ◽  
Angiotensin Ii ◽  
Reversal Potential ◽  
Niflumic Acid ◽  
Channel Blockers ◽  
Ang Ii ◽  
Vasa Recta ◽  
Cell Recording ◽  
Inward Currents

Using nystatin perforated-patch whole cell recording, we investigated the role of Cl−conductance in the modulation of outer medullary descending vasa recta (OMDVR) pericyte membrane potential (Ψm) by ANG II. ANG II (10−11 to 10−7 M) consistently depolarized OMDVR and induced Ψm oscillations at lower concentrations. The Cl− channel blockers anthracene-9-decarboxylate (1 mM) and niflumic acid (10 μM) hyperpolarized resting pericytes and repolarized ANG II-treated pericytes. In voltage-clamp experiments, ANG II-treated pericytes exhibited slowly activating currents that were nearly eliminated by treatment with niflumic acid (10 μM) or removal of extracellular Ca2+. Those currents reversed at −31 and −10 mV when extracellular Cl− concentration was 152 and 34 mM, respectively. In pericytes held at −70 mV, oscillating inward currents were sometimes observed; the reversal potential also shifted with extracellular Cl− concentration. We conclude that ANG II activates a Ca2+-dependent Cl− conductance in OMDVR pericytes to induce membrane depolarization and Ψm oscillations.

scholarly journals Angiotensin II and the Renal Hemodynamic Response to an Isolated Increased Renal Venous Pressure in Rats

2021 ◽  
Vol 12 ◽  
Author(s):  
Xiaohua Huang ◽  
Shereen M. Hamza ◽  
Wenqing Zhuang ◽  
William A. Cupples ◽  
Branko Braam
Keyword(s):  
Angiotensin Ii ◽  
Ace Inhibitor ◽  
Venous Pressure ◽  
Ace Inhibition ◽  
Hemodynamic Response ◽  
Systemic Effect ◽  
Ang Ii ◽  
Renal Vasoconstriction ◽  
Renal Hemodynamic ◽  
Renal Vascular

Elevated central venous pressure increases renal venous pressure (RVP) which can affect kidney function. We previously demonstrated that increased RVP reduces renal blood flow (RBF), glomerular filtration rate (GFR), and renal vascular conductance (RVC). We now investigate whether the RAS and RBF autoregulation are involved in the renal hemodynamic response to increased RVP. Angiotensin II (ANG II) levels were clamped by infusion of ANG II after administration of an angiotensin-converting enzyme (ACE) inhibitor in male Lewis rats. This did not prevent the decrease in ipsilateral RBF (−1.9±0.4ml/min, p<0.05) and GFR (−0.77±0.18ml/min, p<0.05) upon increased RVP; however, it prevented the reduction in RVC entirely. Systemically, the RVP-induced decline in mean arterial pressure (MAP) was more pronounced in ANG II clamped animals vs. controls (−22.4±4.1 vs. −9.9±2.3mmHg, p<0.05), whereas the decrease in heart rate (HR) was less (−5±6bpm vs. −23±4bpm, p<0.05). In animals given vasopressin to maintain a comparable MAP after ACE inhibition (ACEi), increased RVP did not impact MAP and HR. RVC also did not change (0.018±0.008ml/minˑmmHg), and the reduction of GFR was no longer significant (−0.54±0.15ml/min). Furthermore, RBF autoregulation remained intact and was reset to a lower level when RVP was increased. In conclusion, RVP-induced renal vasoconstriction is attenuated when ANG II is clamped or inhibited. The systemic effect of increased RVP, a decrease in HR related to a mild decrease in blood pressure, is attenuated also during ANG II clamp. Last, RBF autoregulation remains intact when RVP is elevated and is reduced to lower levels of RBF. This suggests that in venous congestion, the intact RBF autoregulation could be partially responsible for the vasoconstriction.

Potentiated cortisol response to paired hemorrhage: role of angiotensin and vasopressin

1989 ◽  
Vol 257 (1) ◽  
pp. R118-R126
Author(s):  
M. P. Lilly ◽  
E. J. DeMaria ◽  
T. O. Bruhn ◽  
D. S. Gann
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin ◽  
The Other ◽  
Cortisol Response ◽  
Cortisol Secretion ◽  
Ang Ii ◽  
Cortisol Responses ◽  
The Difference ◽  
Time Courses

Potentiated adrenocorticotropin (ACTH) and cortisol responses occur after the second of two small hemorrhages (hems) spaced 24 h apart in the dog. To test whether increased responses of other hormones might be associated with this effect, we examined plasma renin activity (PRA), angiotensin II (ANG II), and vasopressin after paired 10% hem (H1 and H2) spaced 5 h apart in chronically prepared conscious dogs. Cortisol secretion increased after each hem, and the response to H2 was larger (P less than 0.05; H1 peak at 6.8 +/- 1.3 micrograms/min vs. H2 peak at 18.3 +/- 5.3 micrograms/min). ACTH did not change after H1 but increased after H2, and the H2 response was larger (P less than 0.01). Vasopressin increased after each hem, and the H2 response was larger (P less than 0.01). The time courses of ACTH and vasopressin responses were similar after H2 (significant increases by 8 min). PRA and ANG II increased by 4 min after each hem, and although the difference was small the early PRA and ANG II responses were greater after H2. Blood volume and hem volume did not differ between hems. Hemodynamic responses to the hems were not different. We conclude that, although the PRA and ANG II respond rapidly enough after hem to influence pituitary responses, the slightly greater responses of these factors to H2 are not responsible for greatly increased pituitary-adrenal responses to H2. On the other hand, the markedly potentiated vasopressin response to H2, which parallels that of ACTH, suggests that vasopressin may mediate the increased ACTH responses to H2.

scholarly journals Role of angiotensin II (Ang II) in the hypertension and renal hemodynamic changes in rats with an altered nephrogenesis. Age‐ and sex‐dependent differences

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
F. Javier Salazar ◽  
Virginia Reverte ◽  
Antonio Tapia ◽  
Juan Gambini ◽  
Ignacio Gimenez ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Ang Ii ◽  
Hemodynamic Changes ◽  
Renal Hemodynamic ◽  
Age And Sex

scholarly journals Thromboxane mediates renal hemodynamic response to infused angiotensin II

1991 ◽  
Vol 40 (6) ◽  
pp. 1090-1097 ◽  
Author(s):  
Christopher S. Wilcox ◽  
William J. Welch ◽  
Harold Snellen
Keyword(s):  
Angiotensin Ii ◽  
Hemodynamic Response ◽  
Renal Hemodynamic

Vasoconstriction of outer medullary vasa recta by angiotensin II is modulated by prostaglandin E2

1994 ◽  
Vol 266 (6) ◽  
pp. F850-F857 ◽  
Author(s):  
T. L. Pallone
Keyword(s):  
Angiotensin Ii ◽  
Prostaglandin E2 ◽  
Regional Blood Flow ◽  
Renal Medulla ◽  
Hydraulic Pressure ◽  
Vascular Bundles ◽  
Ang Ii ◽  
Vasa Recta ◽  
Anatomical Arrangement

Vasa recta were dissected from outer medullary vascular bundles in the rat and perfused in vitro. Examination by transmission electron microscopy reveals them to be only outer medullary descending vasa recta (OM-DVR). To establish a method for systematic examination of vasoconstriction, OMDVR were perfused at 5 nl/min with collection pressure increased to 5 mmHg. Under these conditions, transmembrane volume flux was found to be near zero, and the transmural hydraulic pressure gradient was found to be < 15 mmHg. Over a concentration range of 10(-12) to 10(-8) M, abluminal application of angiotensin II (ANG II) caused graded focal vasoconstriction of OMDVR that is blocked by saralasin. Luminal application of ANG II over the same concentration range was much less effective. Abluminal application of prostaglandin E2 (PGE2) shifted the vasoconstrictor response of OMDVR to higher ANG II concentrations. PGE2 reversibly dilated OMDVR that had been preconstricted by ANG II. These results demonstrate that OMDVR are vasoactive segments. Their anatomical arrangement suggests that they play a key role in the regulation of total and regional blood flow to the renal medulla.

Abstract 070: AntagomiR-762 Prevents Angiotensin II Induced Aortic Fibrosis and Stiffening

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Kim Ramil C Montaniel ◽  
Jing Wu ◽  
Matthew R Bersi ◽  
Liang Xiao ◽  
Hana A Itani ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Organ Damage ◽  
Matrix Proteins ◽  
Locked Nucleic Acid ◽  
Ang Ii ◽  
End Organ Damage ◽  
Acid Inhibitor ◽  
Vascular Stiffening ◽  
Aortic Stiffening

We and others have shown that hypertension (HTN) is associated with a striking deposition of collagen in the vascular adventitia. This causes vascular stiffening, which increases pulse wave velocity and contributes to end-organ damage. Through a screen of vascular microRNAs (miRNAs), we found that miR-762 is the most upregulated miRNA in mice with angiotensin II (Ang II)-induced HTN. qRT-PCR confirmed that miR-762 is upregulated 6.35±1.22 (p=0.03) fold in aortas of Ang II-infused mice compared with controls. This was a direct effect of Ang II, as miR-762 upregulation was not eliminated by lowering blood pressure with hydralazine and hydrochlorothiazide and was increased only 2-fold in DOCA salt HTN. To study the role of miR-762 in HTN, we administered a locked nucleic acid inhibitor of miR-762 (antagomiR-762). AntagomiR-762 administration did not alter the hypertensive response to Ang II, yet it normalized stress-strain relationships and aortic energy storage that occurs in systole (Table). Further studies showed that antagomiR-762 dramatically affected vascular matrix proteins, reducing mRNA for several collagens and fibronectin and dramatically upregulating collagenases MMP1a, 8 and 13 (Table). Thus, miR-762 has a major role in modulating vascular stiffening and its inhibition dramatically inhibits pathological fibrosis, enhances matrix degradation and normalizes aortic stiffness. AntagomiR-762 might represent a new approach to prevent aortic stiffening and its consequent end-organ damage.

Reactive Oxygen Species-Mediated Homologous Downregulation of Angiotensin II Type 1 Receptor Mrna by Angiotensin II

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 688-688
Author(s):  
Toshihiro Ichiki ◽  
Kotaro Takeda ◽  
Akira Takeshita
Keyword(s):  
Reactive Oxygen Species ◽  
Angiotensin Ii ◽  
Nadph Oxidase ◽  
Mrna Expression ◽  
Crucial Role ◽  
Oxygen Species ◽  
Ang Ii ◽  
Stimulation Of

58 Recent studies suggest a crucial role of reactive oxygen species (ROS) for the signaling of Angiotensin II (Ang II) through type 1 Ang II receptor (AT1-R). However, the role of ROS in the regulation of AT1-R expression has not been explored. In this study, we examined the effect of an antioxidant on the homologous downregulation of AT1-R by Ang II. Ang II (10 -6 mol/L) decreased AT1-R mRNA with a peak suppression at 6 hours of stimulation in rat aortic vascular smooth muscle cells (VSMC). Ang II dose-dependently (10 -8 -10 -6 ) suppressed AT1-R mRNA at 6 hours of stimulation. Preincubation of VSMC with N-acetylcysteine (NAC), a potent antioxidant, almost completely inhibited the Ang II-induced downregulation of AT1-R mRNA. The effect of NAC was due to stabilization of the AT1-R mRNA that was destabilized by Ang II. Ang II did not affect the promoter activity of AT1-R gene. Diphenylene iodonium (DPI), an inhibitor of NADH/NADPH oxidase failed to inhibit the Ang II-induced AT1-R mRNA downregulation. The Ang II-induced AT1-R mRNA downregulation was also blocked by PD98059, an extracellular signal-regulated protein kinase (ERK) kinase inhibitor. Ang II-induced ERK activation was inhibited by NAC as well as PD98059 whereas DPI did not inhibit it. To confirm the role of ROS in the regulation of AT1-R mRNA expression, VSMC were stimulated with H 2 O 2 . H 2 O 2 suppressed the AT1-R mRNA expression and activated ERK. These results suggest that production of ROS and activation of ERK are critical for downregulation of AT1-R mRNA. The differential effect of NAC and DPI on the downregulation of AT1-R mRNA may suggest the presence of other sources than NADH/NADPH oxidase pathway for ROS in Ang II signaling. Generation of ROS through stimulation of AT1-R not only mediates signaling of Ang II but may play a crucial role in the adaptation process of AT1-R to the sustained stimulation of Ang II.

The effects of estradiol and testosterone on renal tissues oxidative after central injection of angiotensin II in female doca – salt treated rats

2018 ◽  
Vol 37 (3) ◽  
Author(s):  
Marzieh Kafami ◽  
Mahmoud Hosseini ◽  
Saeed Niazmand ◽  
Esmaeil Farrokhi ◽  
Mosa Al-Reza Hajzadeh ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Sex Hormones ◽  
Active Oxygen Species ◽  
Oxygen Species ◽  
Research Needs ◽  
Ang Ii ◽  
Detailed Mechanism ◽  
Female Wistar Rats

Abstract Background Although numerous studies have proven that estrogen (Est) has a protective effect on the development of hypertension, more research needs to be done to show its detailed mechanism in a variety of hypertension. The important role of active oxygen species in blood pressure is well defined. We examined whether or not sex hormones change the growth of reactive oxygen species (ROS) ‎in kidneys after central microinjection of angiotensin II (Ang II).‎ Materials and methods Female Wistar rats, 8 weeks old (200 ± 10 g) were used in this study. The animal groups were (1) Sham, (2) Ovariectomy (OVX), (3) Sham-Hypertension (Sham-Hyper), (4) OVX-Hypertension (OVX-Hyper), (5) Sham-Hyper-Est, (6) OVX-Hyper-Est‎;‎ (7) Sham-Hyper-Testosterone (Tst) and (8) OVX-Hyper-Tst. Solutions of 1% NaCl and 0.1 KCl ‎were used and desoxycorticostrone (doca-salt) was injected (45 mg/kg) 3 times a week in Hypertension groups. Estradiol and Tst (2 mg/kg and ‎5 mg/kg‎; daily; subcutaneously) for 4 weeks. Ang II (50 μM, 5 μL) was microinjected by intracerebroventricular ( i.c.v.) infusion and malondialdehyde (MDA) and thiol in the kidneys were measured. Results MDA in the kidneys was increased by Ang II and doca-salt treatments. Both estradiol and Tst decreased the kidney’s MDA. The level of thiol was higher in Hyper ‎groups and reversed after treatment with estradiol and Tst. Conclusions Our findings suggest that central effect of Ang II on blood pressure and kidney ‎disease is accompanied with increased levels of oxidative stress in the kidneys. Indeed sex hormones change the ROS level in the kidneys after central ‎microinjection of Ang II.‎‎

Renal hemodynamic responses to increased renal venous pressure: role of angiotensin II

1982 ◽  
Vol 243 (3) ◽  
pp. F260-F264 ◽  
Author(s):  
P. R. Kastner ◽  
J. E. Hall ◽  
A. C. Guyton
Keyword(s):  
Angiotensin Ii ◽  
Filtration Rate ◽  
Enzyme Inhibitor ◽  
Venous Pressure ◽  
Renin Secretion ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Filtration Fraction ◽  
A Value

Studies were performed to quantitate the effects of progressive increases in renal venous pressure (RVP) on renin secretion (RS) and renal hemodynamics. RVP was raised in 10 mmHg increments to 50 mmHg. Renin secretion rate increased modestly as RVP was increased to 30 mmHg and then increased sharply after RVP exceeded 30 mmHg. Glomerular filtration rate (GFR), renal blood flow (RBF), and filtration fraction (FF) did not change significantly when RVP was elevated to 50 mmHg. GFR and RBF were also measured after the renin-angiotension system (RAS) was blocked with the angiotensin converting enzyme inhibitor (CEI) SQ 14225. After a 60-min CEI infusion, RBF was elevated (32%), GFR was unchanged, FF was decreased, and total renal resistance (TRR) was decreased. As RVP was increased to 50 mmHg, GFR and FF decreased to 36.3 and 40.0% of control, respectively, RBF returned to a value not significantly different from control, and TRR decreased to 44.8% of control. The data indicate that the RAS plays an important role in preventing reductions in GFR during increased RVP because blockade of angiotensin II (ANG II) formation by the CEI results in marked decreases in GFR at high RVPs. The decreases in GFR after ANG II blockade and RVP elevation were not due to lack of renal vasodilation, since TRR was maintained below while RBF was maintained either above or at the pre-CEI levels.

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