Role of substance P in blood pressure regulation in salt-dependent experimental hypertension.
Hypertension
; 29(1 Pt 2): 506-9, 1997 Jan.
Article
em En
| MEDLINE
| ID: mdl-9039150
ABSTRACT
The participation of substance P in the pathogenesis of five models of experimental hypertension, ie, DOCA-salt, subtotal nephrectomy, one-kidney-one clip renovascular, two-kidney-one clip renovascular, and spontaneous hypertension, was evaluated via an acute infusion of a newly synthesized potent, specific nonpeptide antagonist of substance P at the NK-1 receptor, the agent CP 96,345. In conscious unrestrained rats, CP 96,345 induced significant and sustained increases in mean arterial pressure of DOCA-salt, subtotal nephrectomy, and one-kidney-one clip renovascular hypertensive rats but only small and nonsignificant changes in blood pressure of two-kidney-one clip renovascular and spontaneously hypertensive rats. CP 96,345 had no effect on the blood pressure of sham-treated controls and Wistar-Kyoto rats. This NK-1 receptor antagonist did not significantly affect the heart rate of any experimental model studied. The data suggest that endogenous substance P may act as a partial counterregulatory mechanism against vasoconstriction in models of salt-dependent hypertension.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Vasodilatadores
/
Compostos de Bifenilo
/
Pressão Sanguínea
/
Substância P
/
Antagonistas dos Receptores de Neurocinina-1
/
Hipertensão
Limite:
Animals
Idioma:
En
Revista:
Hypertension
Ano de publicação:
1997
Tipo de documento:
Article
País de afiliação:
Brasil