Knockout of angiotensin 1-7 receptor Mas worsens the course of two-kidney, one-clip Goldblatt hypertension: roles of nitric oxide deficiency and enhanced vascular responsiveness to angiotensin II

Rakusan, D.; Buergelova, M.; Vaneckova, I.; Vanourkova, Z.; Huskova, Z.; Skaroupkova, P.; Mrazova, I.; Opocensky, M.; Kramer, H.J.; Netuka, I.; Maly, J.; Alenina, N.; Bader, M.; Santos, R.A.S.; Cervenka, L.

Knockout of angiotensin 1-7 receptor Mas worsens the course of two-kidney, one-clip Goldblatt hypertension: roles of nitric oxide deficiency and enhanced vascular responsiveness to angiotensin II

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Item Type:	Article
Title:	Knockout of angiotensin 1-7 receptor Mas worsens the course of two-kidney, one-clip Goldblatt hypertension: roles of nitric oxide deficiency and enhanced vascular responsiveness to angiotensin II
Creators Name:	Rakusan, D., Buergelova, M., Vaneckova, I., Vanourkova, Z., Huskova, Z., Skaroupkova, P., Mrazova, I., Opocensky, M., Kramer, H.J., Netuka, I., Maly, J., Alenina, N., Bader, M., Santos, R.A.S. and Cervenka, L.
Abstract:	Aims: The present study was performed to evaluate the effects of target disruption of the G-protein-coupled receptor Mas for angiotensin 1-7 [Ang(1-7)] in knockout mice on the course of two-kidney, one-clip (2K1C) Goldblatt hypertension. Methods: Knockout and wild-type mice underwent clipping of one renal artery. Blood pressure (BP) was monitored by radiotelemetry. The mice were either untreated or chronically treated with the superoxide (O(2)(-)) scavenger tempol (400 mg/l) or the inhibitor of NADPH oxidase apocynin (1 g/l) administered in drinking water. Results: Knockout mice responded to clipping by accelerated increases in BP and the final BP was significantly higher than that in wild-type mice. Chronic treatment with tempol or apocynin elicited similar antihypertensive effects in 2K1C/knockout as in 2K1C/wild-type mice. Acute nitric oxide synthase inhibition caused greater BP increases in 2K1C/wild-type than in 2K1C/knockout mice. Conclusion: Our present findings support the notion that the angiotensin-converting enzyme 2-Ang(1-7)-Mas axis serves as an important endogenous physiological counterbalancing mechanism that partially attenuates the hypertensinogenic actions of the activated renin-angiotensin system. The impairment in this axis may contribute to the deterioration of the course of 2K1C Goldblatt hypertension.
Keywords:	Two-kidney, one-clip Goldblatt hypertension, Mas Receptor Knockout Mice, Nitric Oxide Deficiency, Animals, Mice
Source:	Kidney and Blood Pressure Research
ISSN:	1420-4096
Publisher:	Karger
Volume:	33
Number:	6
Page Range:	476-488
Date:	December 2010
Official Publication:	https://doi.org/10.1159/000320689
PubMed:	View item in PubMed

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