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Titolo:
ROLE OF ANGIOTENSIN-II AND BRADYKININ ON AORTIC COLLAGEN FOLLOWING CONVERTING-ENZYME INHIBITION IN SPONTANEOUSLY HYPERTENSIVE RATS
Autore:
BENETOS A; LEVY BI; LACOLLEY P; TAILLARD F; DURIEZ M; SAFAR ME;
Indirizzi:
HOP BROUSSAIS,96 RUE DIDOT F-75674 PARIS 14 FRANCE INSERM,U337 PARIS FRANCE INSERM,U141 PARIS FRANCE
Titolo Testata:
Arteriosclerosis, thrombosis, and vascular biology
fascicolo: 11, volume: 17, anno: 1997,
pagine: 3196 - 3201
SICI:
1079-5642(1997)17:11<3196:ROAABO>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
PRESSURE-OVERLOAD HYPERTROPHY; SMOOTH-MUSCLE CELLS; ENDOGENOUS BRADYKININ; CARDIAC-HYPERTROPHY; RECEPTOR ANTAGONIST; BLOOD-PRESSURE; LEFT-VENTRICLE; BLOCKADE; STIFFNESS; PREVENTS;
Keywords:
AORTIC HYPERTROPHY; BRADYKININ RECEPTOR ANTAGONIST; COLLAGEN; ANGIOTENSIN II RECEPTOR ANTAGONIST;
Tipo documento:
Article
Natura:
Periodico
Citazioni:
49
Recensione:
Indirizzi per estratti:
Citazione:
A. Benetos et al., "ROLE OF ANGIOTENSIN-II AND BRADYKININ ON AORTIC COLLAGEN FOLLOWING CONVERTING-ENZYME INHIBITION IN SPONTANEOUSLY HYPERTENSIVE RATS", Arteriosclerosis, thrombosis, and vascular biology, 17(11), 1997, pp. 3196-3201

Abstract

We previously showed that chronic angiotensin-converting enzyme (ACE)inhibition prevented the increase in aortic collagen in spontaneouslyhypertensive rats (SHRs) independently of blood pressure reduction. The aim of the present study was to determine whether the effects of ACE inhibition on aortic fibrosis were due to inhibition of angiotensin II formation, preservation of bradykinin, or a combination of both. Four week-old SHRs were treated for 4 months with the ACE inhibitor quinapril, quinapril with the bradykinin B-2 receptor antagonist Hoe 140, or the angiotensin II AT(1) receptor antagonist CI996. Control SHR andWistar-Kyoto (WKY) rats received a placebo for the same period of time. At the end of the treatment, as compared to conscious SHR and WKY controls, quinapril completely prevented the development of hypertension, whereas quinapril-Hoe 140 and the AT(1) receptor antagonist produced only a partial reduction of blood pressure. In relation with blood pressure changes, aortic hypertrophy was significantly prevented by quinapril but not by quinapril-Hoe 140 or CI996. In contrast, aortic collagen accumulation was completely prevented by all three treatments. The study provides evidence that in young live SHRs, the prevention of aortic collagen accumulation is independent of blood pressure changes and bradykinin preservation and involves exclusively angiotensin II inhibition through AT(1) receptors.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 31/03/20 alle ore 21:39:30