Pregnancy induced angiotensin II Type-1 receptor expression in ovine uterine artery does not involve formation of alternate splice variants or alternate promoter usage

1998 ◽  
Vol 5 (1) ◽  
pp. 144A-144A
Author(s):  
I BIRD ◽  
D MILLICAN ◽  
R MAGNESS
2013 ◽  
Vol 1 (5) ◽  
Author(s):  
Jason A. Collett ◽  
Anne K. Hart ◽  
Elaine Patterson ◽  
Julie Kretzer ◽  
Jeffrey L. Osborn

The Prostate ◽  
2011 ◽  
Vol 71 (14) ◽  
pp. 1510-1517 ◽  
Author(s):  
Takeo Kosaka ◽  
Akira Miyajima ◽  
Suguru Shirotake ◽  
Eiji Kikuchi ◽  
Mototsugu Oya

2000 ◽  
Vol 278 (2) ◽  
pp. H353-H359 ◽  
Author(s):  
Donna S. Lambers ◽  
Suzanne G. Greenberg ◽  
Kenneth E. Clark

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.


Peptides ◽  
2020 ◽  
Vol 133 ◽  
pp. 170384
Author(s):  
Débora Raupp ◽  
Renata Streck Fernandes ◽  
Krist Helen Antunes ◽  
Fabíola Adélia Perin ◽  
Katya Rigatto

2000 ◽  
Vol 6 (S2) ◽  
pp. 618-619
Author(s):  
P. Y. Lau ◽  
M. G. Cardarelli ◽  
C. Wei

Angiotensin II (AH) is a potent vasoconstrictor and mitogenic factor. AH receptors include type 1 (ATI) and type 2 (AT2) receptors. Recent studies demonstrated that both ATI and AT2 receptors expressed in human myocardium. Circulating and local tissue level of AH was increased in severe congestive heart failure (CHF). However, the expression of ATI and AT2 in cardiac tissue with CHF remains controversial. Therefore, the present study was designed to investigate the protein expression of ATI and AT2 receptors in normal human myocardium and in human cardiac tissue with mild and severe CHF.Human atrial tissues from normal subjects and CHF patients with ischemic cardiomyopathy and dilated cardiomyopathy were obtained from open-heart surgery and cardiac transplantation. ATI and AT2 receptor expression was investigated by immunohistochemical staining (IHCS). The results of IHCS was evaluated by IHCS staining density scores (0, no staining; 1, minimal staining; 2, mild staining; 3, moderate staining; and 4, strong staining).


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