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Intrarenal alterations of the angiotensin-converting enzyme type 2/angiotensin 1-7 complex of the renin-angiotensin system do not alter the course of malignant hypertension in Cyp1a1-Ren-2 transgenic rats
Z. Husková, L. Kopkan, L. Červenková, Š. Doleželová, Z. Vaňourková, P. Škaroupková, A. Nishiyama, E. Kompanowska-Jezierska, J. Sadowski, HJ. Kramer, L. Červenka,
Jazyk angličtina Země Austrálie
Typ dokumentu časopisecké články, práce podpořená grantem
Grantová podpora
NT14085
MZ0
CEP - Centrální evidence projektů
Digitální knihovna NLK
Plný text - Článek
Zdroj
NLK
Medline Complete (EBSCOhost)
od 1998-01-01 do Před 1 rokem
PubMed
26833491
DOI
10.1111/1440-1681.12553
Knihovny.cz E-zdroje
- MeSH
- aktivátory enzymů farmakologie MeSH
- albuminurie komplikace MeSH
- angiotensin I metabolismus MeSH
- angiotensin konvertující enzym metabolismus MeSH
- cytochrom P-450 CYP1A1 genetika MeSH
- diminazen analogy a deriváty farmakologie MeSH
- hypertenze maligní komplikace metabolismus patofyziologie moč MeSH
- krevní tlak účinky léků MeSH
- krysa rodu rattus MeSH
- ledviny účinky léků metabolismus MeSH
- myši MeSH
- peptidové fragmenty metabolismus MeSH
- peptidy farmakologie MeSH
- potkani transgenní MeSH
- regulace genové exprese účinky léků MeSH
- renin-angiotensin systém účinky léků MeSH
- renin genetika MeSH
- sodík moč MeSH
- tělesná hmotnost účinky léků MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
The role of the intrarenal renin-angiotensin system (RAS) in the pathophysiology of malignant hypertension is not fully understood. Accumulating evidence indicates that the recently discovered vasodilator axis of the RAS, angiotensin-converting enzyme (ACE) type 2 (ACE2)/angiotensin 1-7 (ANG 1-7), constitutes an endogenous system counterbalancing the hypertensiogenic axis, ACE/angiotensin II (ANG II)/AT1 receptor. This study aimed to evaluate the role of the intrarenal vasodilator RAS axis in the pathophysiology of ANG II-dependent malignant hypertension in Cyp1a1-Ren-2 transgenic rats. ANG II-dependent malignant hypertension was induced by 13 days' dietary administration of indole-3-carbinol (I3C), a natural xenobiotic that activates the mouse renin gene in Cyp1a1-Ren-2 transgenic rats. It was hypothesized that pharmacologically-induced inhibition of the ACE2/ANG 1-7 complex should aggravate, and activation of this axis should attenuate, the course of ANG II-dependent malignant hypertension. Blood pressure (BP) was monitored by radiotelemetry. ACE2 inhibitor (DX 600, 0.2 μg/day) and ACE2 activator (DIZE, 1 mg/day) were administrated via osmotic minipumps. Even though ACE2 inhibitor significantly decreased and ACE2 activator increased intrarenal ANG 1-7 concentrations, the course of BP, as well as of albuminuria, cardiac hypertrophy and renal glomerular damage, were not altered. It was shown that intrarenal alterations in the ACE2/ANG 1-7 complex did not significantly modify the course of malignant hypertension in I3C-induced Cyp1a1-Ren-2 transgenic rats. Thus, in our experimental setting alterations of this intrarenal vasodilator complex of the RAS do not significantly modify the form of malignant hypertension that clearly depends on the inappropriately increased activity of the ACE/ANG II/AT1 receptor axis.
Department of Pharmacology Kagawa University Kagawa Japan
Section of Nephrology Department of Medicine University of Bonn Bonn Germany
Citace poskytuje Crossref.org
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