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Vasodepressor role of endogenous bradykinin assessed by a bradykinin antagonist.
Author(s) -
A Benetos,
Haralambos Gavras,
John M. Stewart,
Raymond J. Vavrek,
S Hatinoglou
Publication year - 1986
Publication title -
hypertension
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.986
H-Index - 265
eISSN - 1524-4563
pISSN - 0194-911X
DOI - 10.1161/01.hyp.8.11.971
Subject(s) - bradykinin , bradykinin receptor , enalapril , renovascular hypertension , saralasin , sodium nitroprusside , antagonist , blood pressure , medicine , endocrinology , enzyme inhibitor , ace inhibitor , angiotensin converting enzyme , pharmacology , chemistry , renin–angiotensin system , enzyme , nitric oxide , receptor , biochemistry
This study was designed to examine the contribution of bradykinin to the depressor effect of different antihypertensive drugs in two-kidney renovascular hypertensive rats, using a new specific antagonist of bradykinin. First, the inhibitory capacity of this peptide for exogenously injected bradykinin (75-200 ng) was tested. An inhibition of the vasodepressor action of bradykinin by over 50% was found when the bradykinin inhibitor was infused at a rate of 40 micrograms/min, with little difference at higher rates of infusion. This inhibitor then was infused in three groups of renovascular hypertensive rats after their blood pressure had been decreased by pretreatment with the converting enzyme inhibitor enalapril (MK 421), saralasin, or sodium nitroprusside, respectively. Infusion of the inhibitor produced an immediate 30% increase in blood pressure only in the enalapril-treated group. These results indicate that bradykinin is involved in the decrease of blood pressure produced by converting enzyme inhibition in experimental renovascular hypertension.

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