Combined suppression of the intrarenal and circulating vasoconstrictor renin-ACE-ANG II axis and augmentation of the vasodilator ACE2-ANG 1-7-Mas axis attenuates the systemic hypertension in Ren-2 transgenic rats exposed to chronic hypoxia
Jazyk angličtina Země Česko Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
25194129
DOI
10.33549/physiolres.932842
PII: 932842
Knihovny.cz E-zdroje
- MeSH
- angiotensin I krev MeSH
- angiotensin II krev MeSH
- angiotensin konvertující enzym krev MeSH
- angiotensin-konvertující enzym 2 MeSH
- hypertenze krev genetika patofyziologie prevence a kontrola MeSH
- hypoxie komplikace enzymologie patofyziologie MeSH
- krevní tlak MeSH
- ledviny enzymologie MeSH
- modely nemocí na zvířatech MeSH
- peptidové fragmenty krev MeSH
- potkani Sprague-Dawley MeSH
- potkani transgenní MeSH
- protoonkogen Mas MeSH
- protoonkogenní proteiny krev MeSH
- receptory spřažené s G-proteiny krev MeSH
- renin-angiotensin systém * MeSH
- renin krev genetika MeSH
- signální transdukce MeSH
- vazodilatace * MeSH
- vazokonstrikce * MeSH
- věkové faktory MeSH
- zvířata MeSH
- Check Tag
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- Ace2 protein, mouse MeSH Prohlížeč
- Ace2 protein, rat MeSH Prohlížeč
- angiotensin I (1-7) MeSH Prohlížeč
- angiotensin I MeSH
- angiotensin II MeSH
- angiotensin konvertující enzym MeSH
- angiotensin-konvertující enzym 2 MeSH
- peptidové fragmenty MeSH
- protoonkogen Mas MeSH
- protoonkogenní proteiny MeSH
- receptory spřažené s G-proteiny MeSH
- Ren2 protein, mouse MeSH Prohlížeč
- renin MeSH
The aim of the present study was to test the hypothesis that chronic hypoxia would aggravate hypertension in Ren-2 transgenic rats (TGR), a well-defined monogenetic model of hypertension with increased activity of endogenous renin-angiotensin system (RAS). Systolic blood pressure (SBP) in conscious rats and mean arterial pressure (MAP) in anesthetized TGR and normotensive Hannover Sprague-Dawley (HanSD) rats were determined under normoxia that was either continuous or interrupted by two weeks´ hypoxia. Expression, activities and concentrations of individual components of RAS were studied in plasma and kidney of TGR and HanSD rats under normoxic conditions and after exposure to chronic hypoxia. In HanSD rats two weeks´ exposure to chronic hypoxia did not alter SBP and MAP. Surprisingly, in TGR it decreased markedly SBP and MAP; this was associated with substantial reduction in plasma and kidney renin activities and also of angiotensin II (ANG II) levels, without altering angiotensin-converting enzyme (ACE) activities. Simultaneously, in TGR the exposure to hypoxia increased kidney ACE type 2 (ACE2) activity and angiotensin 1-7 (ANG 1-7) concentrations as compared with TGR under continuous normoxia. Based on these results, we propose that suppression of the hypertensiogenic ACE-ANG II axis in the circulation and kidney tissue, combined with augmentation of the intrarenal vasodilator ACE2-ANG 1-7 axis, is the main mechanism responsible for the blood pressure-lowering effects of chronic hypoxia in TGR.
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