In:
Kidney and Blood Pressure Research, S. Karger AG, Vol. 33, No. 6 ( 2010), p. 476-488
Abstract:
〈 i 〉 Aims: 〈 /i 〉 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. 〈 i 〉 Methods: 〈 /i 〉 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 〈 sub 〉 2 〈 /sub 〉 〈 sup 〉 – 〈 /sup 〉 ) scavenger tempol (400 mg/l) or the inhibitor of NADPH oxidase apocynin (1 g/l) administered in drinking water. 〈 i 〉 Results: 〈 /i 〉 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. 〈 i 〉 Conclusion: 〈 /i 〉 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.
Type of Medium:
Online Resource
ISSN:
1420-4096
,
1423-0143
Language:
English
Publisher:
S. Karger AG
Publication Date:
2010
detail.hit.zdb_id:
1482922-8
