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
Language English Country Switzerland Media print-electronic
Document type Comparative Study, Journal Article, Research Support, Non-U.S. Gov't
PubMed
21071955
DOI
10.1159/000320689
PII: 000320689
Knihovny.cz E-resources
- MeSH
- Angiotensin I deficiency genetics MeSH
- Angiotensin II physiology MeSH
- Surgical Instruments MeSH
- Blood Pressure drug effects physiology MeSH
- Mice, Knockout MeSH
- Mice MeSH
- Nitric Oxide deficiency physiology MeSH
- Peptide Fragments deficiency genetics MeSH
- Disease Progression * MeSH
- Proto-Oncogene Mas MeSH
- Proto-Oncogene Proteins deficiency genetics MeSH
- Receptors, G-Protein-Coupled deficiency genetics MeSH
- Hypertension, Renovascular genetics metabolism pathology MeSH
- Vasomotor System drug effects physiology MeSH
- Animals MeSH
- Check Tag
- Male MeSH
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Comparative Study MeSH
- Names of Substances
- angiotensin I (1-7) MeSH Browser
- Angiotensin I MeSH
- Angiotensin II MeSH
- Nitric Oxide MeSH
- Peptide Fragments MeSH
- Proto-Oncogene Mas MeSH
- Proto-Oncogene Proteins MeSH
- Receptors, G-Protein-Coupled MeSH
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.
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