scholarly journals Different Vascular Responses to Subpressor Angiotensin II Administration in the Mesenteric and Renal Circulation of Rats

1996 ◽  
Vol 9 (4) ◽  
pp. 385-392 ◽  
Author(s):  
G Cserep
Keyword(s):  
Angiotensin Ii ◽  
Renal Circulation ◽  
Vascular Responses

Functional role of angiotensin II type 1 and 2 receptors in regulation of uterine blood flow in nonpregnant sheep

2000 ◽  
Vol 278 (2) ◽  
pp. H353-H359 ◽  
Author(s):  
Donna S. Lambers ◽  
Suzanne G. Greenberg ◽  
Kenneth E. Clark
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Uterine Artery ◽  
Receptor Subtype ◽  
Ang Ii ◽  
Uterine Blood Flow ◽  
Response Curves ◽  
Vascular Responses

The objective was to determine the receptor subtype of angiotensin II (ANG II) that is responsible for vasoconstriction in the nonpregnant ovine uterine and systemic vasculatures. Seven nonpregnant estrogenized ewes with indwelling uterine artery catheters and flow probes received bolus injections (0.1, 0.3 and 1 μg) of ANG II locally into the uterine artery followed by a systemic infusion of ANG II at 100 ng ⋅ kg−1 ⋅ min−1for 10 min to determine uterine vasoconstrictor responses. Uterine ANG II dose-response curves were repeated following administration of the ANG II type 2 receptor (AT2) antagonist PD-123319 and then repeated again in the presence of an ANG II type 1 receptor (AT1) antagonist L-158809. In a second experiment, designed to investigate the mechanism of ANG II potentiation that occurred in the presence of AT2 blockade, nonestrogenized sheep received a uterine artery infusion of L-158809 (3 mg/min for 5 min) prior to the infusion of 0.03 μg/min of ANG II for 10 min. ANG II produced dose-dependent decreases in uterine blood flow ( P < 0.03), which were potentiated in the presence of the AT2 antagonist ( P < 0.02). Addition of the AT1 antagonist abolished the uterine vascular responses and blocked ANG II-induced increases in systemic arterial pressure ( P < 0.01). Significant uterine vasodilation ( P < 0.01) was noted with AT1 blockade in the second experiment, which was reversed by administration of the AT2 antagonist or by the nitric oxide synthetase inhibitor N ω-nitro-l-arginine methyl ester. We conclude that the AT1- receptors mediate the systemic and uterine vasoconstrictor responses to ANG II in the nonpregnant ewe. AT2-receptor blockade resulted in a potentiation of the uterine vasoconstrictor response to ANG II, suggesting that the AT2-receptor subtype may modulate uterine vascular responses to ANG II potentially by release of nitric oxide.

scholarly journals Angiotensin II modulates amphetamine‐induced glial and brain vascular responses, and attention deficit via angiotensin type 1 receptor: Evidence from brain regional sensitivity to amphetamine

2020 ◽  
Vol 51 (4) ◽  
pp. 1026-1041 ◽  
Author(s):  
Natalia Andrea Marchese ◽  
Victoria Belén Occhieppo ◽  
Osvaldo Martin Basmadjian ◽  
Brenda Solange Casarsa ◽  
Gustavo Baiardi ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Attention Deficit ◽  
Vascular Responses ◽  
Angiotensin Type

scholarly journals Role of angiotensin II on the adrenal and vascular responses to hemorrhage during development in fetal lambs.

1982 ◽  
Vol 50 (5) ◽  
pp. 645-650 ◽  
Author(s):  
J E Robillard ◽  
R A Gomez ◽  
J G Meernik ◽  
W D Kuehl ◽  
D VanOrden
Keyword(s):  
Angiotensin Ii ◽  
Vascular Responses

Renal medullary plasma flow rate and reabsorption of salt and water from inner medullary collecting duct

1987 ◽  
Vol 65 (12) ◽  
pp. 2415-2421 ◽  
Author(s):  
W. A. Cupples ◽  
H. Sonnenberg
Keyword(s):  
Blood Flow ◽  
Sodium Chloride ◽  
Angiotensin Ii ◽  
Flow Rate ◽  
Plasma Flow ◽  
Collecting Duct ◽  
Urine Osmolality ◽  
Renal Circulation ◽  
Inner Medullary Collecting Duct ◽  
Medullary Collecting Duct

It has been proposed that medullary washout secondary to increased blood flow will limit maximal urine osmolality and reabsorption of salt and water from the inner medullary collecting duct. We have tested this prediction. The function of the inner medullary collecting duct was examined by microcatheterization. Acetylcholine was infused directly into the renal circulation, captopril was infused intravenously, and angiotensin II was infused into the renal circulation in rats which also received captopril. Medullary plasma flow rate, measured by dye–dilution in parallel experiments, was not significantly increased by acetylcholine; it was increased 30% (p < 0.02) by systemic infusion of captopril, and was returned to control by angiotensin II. Acetylcholine increased both urine flow rate and sodium excretion (p < 0.01, p < 0.001, respectively), while captopril increased only sodium excretion (p < 0.025). Angiotensin II blocked the natriuresis due to captopril. None of the treatments altered urine osmolality (p > 0.4 in all cases). Acetylcholine increased the loads of water, sodium, chloride, and total solute delivered to the inner medullary collecting duct. Angiotensin II reduced delivery of water and solutes compared with captopril alone. None of the treatments affected load dependency of reabsorption of water, sodium, chloride, or total solute in the inner medullary collecting duct. We conclude that there is, at most, a weak interaction between medullary blood flow and reabsorption from the inner medullary collecting duct.

scholarly journals Renal Vascular Response to Angiotensin II Administration in Two Kidneys-One Clip Hypertensive Rats Treated with High Dose of Estradiol: The Role of Mas Receptor

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Samira Choopani ◽  
Mehdi Nematbakhsh
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Ovariectomized Rats ◽  
Ang Ii ◽  
Vascular Response ◽  
Hypertensive Rats ◽  
Vascular Responses ◽  
Mas Receptor ◽  
Renal Vascular

Backgrounds. High blood pressure is one of the most important causes of death around the world. The renin-angiotensin system (RAS) and estradiol are two important items that regulate arterial blood pressure in women. However, hypertension, RAS, and sex hormone estradiol may influence renal vascular responses. This study was designed to determine the role of Mas receptor (MasR) on renal vascular response to angiotensin II (Ang II) administration in two kidneys-one clip (2K1C) hypertensive rats treated with estradiol. Method. The ovariectomized rats were subjected to 2K1C or non-2K1C and simultaneously treated with estradiol (500 μg/kg/weekly) or placebo for a period of 4 weeks. Subsequently, under anesthesia, renal vascular responses to graded doses of Ang II administration with MasR blockade (A779) or its vehicle were determined. Results. A779 or its vehicle did not alter mean arterial pressure (MAP), renal perfusion pressure (RPP), and renal blood flow (RBF). However, in non-2K1C rats, Ang II infusion decreased RBF and increased renal vascular resistance (RVR) responses in a dose-related manner ( P treat < 0.0001 ). The greatest responses were found in ovariectomized estradiol-treated rats that received A779 ( P group < 0.05 ) in non-2K1C rats. Such findings were not detected in 2K1C hypertensive rats. For example, in estradiol-treated rats that received A779, at 1000 ng/kg/min of Ang II infusion, RBF reduced from 1.6 ± 0.2 to 0.89 ± 0.19  ml/min in non-2K1C rats, and it reduced from 1.6 ± 0.2 to 1.2 ± 0.2  ml/min in 2K1C rats. Conclusion. Hypertension induced by 2K1C may attenuate the role of A779 and estradiol in renal vascular responses to Ang II infusion. Perhaps, this response can be explained by the reduction of Ang II type 1 receptor (AT1R) expression in the 2K1C hypertensive rats.

Sign in / Sign up

Export Citation Format

Share Document