Hypertensive response to acute aortic coarctation in chronic vasopressin deficient states.
Clin Exp Hypertens
; 17(6): 977-88, 1995 Aug.
Article
em En
| MEDLINE
| ID: mdl-7581264
We investigated the genesis of the hypertensive response to acute (45 min) aortic constriction in two models of chronic vasopressin (AVP) deficiency, i.e., Brattleboro strain and median eminence lesioned (MEL) Wistar rats. The same degree of partial aortic constriction, with a pneumatic cuff placed around the abdominal aorta, yielded a sudden and maintained increase in carotid pressure to the same extent in Brattleboro, MEL and sham-MEL rats. Blockage of AVP V1 receptors with d(CH2)5Tyr[Me]AVP did not affect the hypertensive response of Brattleboro or MEL rats, but gradually blunted the response of sham-MEL rats. Blockage of angiotensin II receptors with saralasin blunted the hypertensive response of the AVP-deficient subjects throughout the experiment, but only delayed (5-15 min) the onset of hypertension in sham-MEL rats. Simultaneous blockage of AVP and angiotensin II blunted the hypertensive response of sham-MEL and AVP-deficient rats throughout the experiment. These data demonstrate that when one vasoactive system is chronically absent, as is the case for AVP in Brattleboro and MEL rats, the renin-angiotensin system plays the major role in the pathophysiology of acute aortic coarctation hypertension.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Coartação Aórtica
/
Arginina Vasopressina
/
Hipertensão
Limite:
Animals
Idioma:
En
Revista:
Clin Exp Hypertens
Ano de publicação:
1995
Tipo de documento:
Article
País de afiliação:
Brasil
País de publicação:
Reino Unido