Plasma and kidney angiotensin II levels and renal functional responses to AT1 receptor blockade in hypertensive Ren-2 transgenic rats

2004 ◽  
Vol 22 (4) ◽  
pp. 819-825 ◽  
Author(s):  
Libor Kopkan ◽  
Herbert J Kramer ◽  
Zuzana Husková ◽  
Zdeňka Vaňourková ◽  
Angela Bäcker ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
At1 Receptor ◽  
Receptor Blockade ◽  
Functional Responses ◽  
Transgenic Rats

scholarly journals Angiotensin Ii Type 1 (at1 ) Receptor Blockade Enhances the L-NAME-Induced Vasoconstriction in Rat Submandibular Gland

2002 ◽  
Vol 87 (3) ◽  
pp. 327-333 ◽  
Author(s):  
J. Vág ◽  
Beáta Kerémi ◽  
Csilla Hably ◽  
J. Bartha ◽  
Á. Fazekas
Keyword(s):  
Angiotensin Ii ◽  
Submandibular Gland ◽  
At1 Receptor ◽  
Receptor Blockade ◽  
Rat Submandibular Gland

scholarly journals Impaired Vascular Contractility and Aortic Wall Degeneration in Fibulin-4 Deficient Mice: Effect of Angiotensin II Type 1 (AT1) Receptor Blockade

PLoS ONE ◽  
2011 ◽  
Vol 6 (8) ◽  
pp. e23411 ◽  
Author(s):  
Els Moltzer ◽  
Luuk te Riet ◽  
Sigrid M. A. Swagemakers ◽  
Paula M. van Heijningen ◽  
Marcel Vermeij ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Aortic Wall ◽  
At1 Receptor ◽  
Receptor Blockade ◽  
Vascular Contractility ◽  
Deficient Mice

AT1 receptor blockade and the sympathoadrenal response to insulin-induced hypoglycemia in humans

1997 ◽  
Vol 272 (3) ◽  
pp. E415-E421 ◽  
Author(s):  
R. H. Worck ◽  
H. Ibsen ◽  
E. Frandsen ◽  
H. Dige-Petersen
Keyword(s):  
Angiotensin Ii ◽  
Time Course ◽  
Forearm Blood Flow ◽  
At1 Receptor ◽  
Receptor Blockade ◽  
Norepinephrine Release ◽  
Short Intervals ◽  
Intravenous Insulin ◽  
Arterial Glucose ◽  
Epinephrine Concentration

An important facilitating effect of angiotensin II on adrenal catecholamine release has been demonstrated in several species. To determine whether specific AT1 receptor blockade affects medullary epinephrine secretion and musculocutaneous norepinephrine release during insulin-induced hypoglycemia, 16 healthy volunteers received losartan vs. placebo followed by an intravenous insulin bolus and measurement of effect variables at short intervals for 150 min. AT1 receptor blockade was effective, as evidenced by substantially increased circulating renin and angiotensin II levels, a 60% inhibition of circulating aldosterone, and an 8.5% decrease of mean arterial pressure over time compared with placebo. Arterial glucose concentration fell to a nadir of 1.9 mM, arterial epinephrine concentration increased 23-fold, forearm musculocutaneous norepinephrine release increased 4-fold, heart rate increased 40%, and forearm blood flow increased 3-fold. All absolute values and the time course of these changes were independent of AT1 receptor blockade. It is concluded that a putative interaction between angiotensin II and the sympathoadrenal axis may not be mediated by AT1 receptors in humans.

scholarly journals Angiotensin II AT1 Receptor Blockade Ameliorates Brain Inflammation

2010 ◽  
Vol 36 (4) ◽  
pp. 857-870 ◽  
Author(s):  
Julius Benicky ◽  
Enrique Sánchez-Lemus ◽  
Masaru Honda ◽  
Tao Pang ◽  
Martina Orecna ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
At1 Receptor ◽  
Brain Inflammation ◽  
Receptor Blockade

Effects of angiotensin II (AT1) receptor blockade on cardiac vagal control in heart failure

2001 ◽  
Vol 101 (6) ◽  
pp. 559-566 ◽  
Author(s):  
J. C. VAILE ◽  
S. CHOWDHARY ◽  
F. OSMAN ◽  
H. F. ROSS ◽  
J. FLETCHER ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Angiotensin Ii ◽  
Baroreflex Sensitivity ◽  
At1 Receptor ◽  
Receptor Blockade ◽  
Double Blind ◽  
Rr Interval

The objective of the present study was to determine the autonomic effects of angiotensin II (AT1) receptor blocker therapy in heart failure. In a randomized double-blind cross-over study, we compared the effects of candesartan and placebo on baroreflex sensitivity and on heart rate variability at rest, during stress and during 24h monitoring. Acute effects were assessed 4h after oral candesartan (8mg) and chronic effects after 4 weeks of treatment (dose titrated to 16mg daily). The study group comprised 21 patients with heart failure [mean (S.E.M.) ejection fraction 33% (1%)], in the absence of angiotensin-converting enzyme (ACE) inhibitor therapy. We found that acute candesartan was not different from placebo in its effects on blood pressure or mean RR interval. Chronic candesartan significantly reduced blood pressure [placebo, 137 (3)/82 (3)mmHg; candesartan, 121 (4)/75 (2)mmHg; P<0.001; values are mean (S.E.M.)], but had no effect on mean RR interval [placebo, 857 (25)ms; candesartan, 857 (21)ms]. Compared with placebo there were no significant effects of acute or chronic candesartan on heart rate variability in the time domain and no consistent effects in the frequency domain. Baroreflex sensitivity assessed by the phenylephrine bolus method was significantly increased after chronic candesartan [placebo, 3.5 (0.5)ms/mmHg; candesartan, 4.8 (0.7)ms/mmHg; P<0.05], although there were no changes in cross-spectral baroreflex sensitivity. Thus, in contrast with previous results with ACE inhibitors, angiotensin II receptor blockade in heart failure did not increase heart rate variability, and there was no consistent effect on baroreflex sensitivity.

scholarly journals Interaction between vasopressin and angiotensin II in vivo and in vitro: effect on aquaporins and urine concentration

2010 ◽  
Vol 299 (3) ◽  
pp. F577-F584 ◽  
Author(s):  
Weidong Wang ◽  
Chunling Li ◽  
Sandra Summer ◽  
Sandor Falk ◽  
Robert W. Schrier
Keyword(s):  
Angiotensin Ii ◽  
Collecting Duct ◽  
Receptor Activation ◽  
Urine Concentration ◽  
At1 Receptor ◽  
Receptor Blockade ◽  
Ang Ii ◽  
Vitro Effect

The study was undertaken to examine the potential cross talk between vasopressin and angiotensin II (ANG II) intracellular signaling pathways. We investigated in vivo and in vitro whether vasopressin-induced water reabsorption could be attenuated by ANG II AT1 receptor blockade (losartan). On a low-sodium diet (0.5 meq/day) dDAVP-treated animals with or without losartan exhibited comparable renal function [creatinine clearance 1.2 ± 0.1 in dDAVP+losartan (LSDL) vs. 1.1 ± 0.1 ml·100 g−1·day−1 in dDAVP alone (LSD), P > 0.05] and renal blood flow (6.3 ± 0.5 in LSDL vs. 6.8 ± 0.5 ml/min in LSD, P > 0.05). The urine output, however, was significantly increased in LSDL (2.5 ± 0.2 vs. 1.8 ± 0.2 ml·100 g−1·day−1, P < 0.05) in association with decreased urine osmolality (2,600 ± 83 vs. 3,256 ± 110 mosmol/kgH2O, P < 0.001) compared with rats in LSD. Immunoblotting revealed significantly decreased expression of medullary AQP2 (146 ± 6 vs. 176 ± 10% in LSD, P < 0.01), p-AQP2 (177 ± 13 vs. 214 ± 12% in LSD, P < 0.05), and AQP3 (134 ± 14 vs. 177 ± 11% in LSD, P < 0.05) in LSDL compared with LSD. The expressions of AQP1, the α1- and γ-subunits of Na-K-ATPase, and the Na-K-2Cl cotransporter were not different among groups. In vitro studies showed that ANG II or dDAVP treatment was associated with increased AQP2 expression and cAMP levels, which were potentiated by cotreatment with ANG II and dDAVP and were inhibited by AT1 blockade. In conclusion, ANG II AT1 receptor blockade in dDAVP-treated rats on a low-salt diet was associated with decreased urine concentration and decreased inner medullary AQP2, p-AQP2, and AQP3 expression, suggesting that AT1 receptor activation plays a significant role in regulating aquaporin expression and modulating urine concentration in vivo. Studies in collecting duct cells were confirmatory.

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