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FACILITATION OF NORADRENERGIC TRANSMISSION BY LOCALLY GENERATED ANGIOTENSIN II IN GUINEA‐PIG ISOLATED ATRIA AND IN THE PERFUSED CAUDAL ARTERY OF THE RAT
Author(s) -
Ziogas J.,
Story D. F.,
Rand M. J.
Publication year - 1984
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1984.tb00290.x
Subject(s) - saralasin , angiotensin ii , enalaprilat , medicine , endocrinology , renin–angiotensin system , angiotensin receptor , angiotensin ii receptor type 1 , stimulation , angiotensin converting enzyme , angiotensin iii , chemistry , guinea pig , biology , receptor , blood pressure , ace inhibitor
SUMMARY 1. In guinea‐pig isolated atria, angiotensin I and angiotensin II produced concentration dependent increases in the rate of spontaneous beating and in the release of noradrenaline produced by field stimulation of sympathetic nerves. 2. In rat isolated caudal artery preparations, both angiotensin I and angiotensin II had direct vasoconstrictor actions and also produced concentration dependent increases in constrictor responses to periarterial sympathetic stimulation. 3. All the above effects of angiotensin I and angiotensin II were blocked by the receptor antagonist saralasin, but only those of angiotensin I were blocked by the converting enzyme inhibitor enalaprilat (MK‐422). 4. The findings confirm that angiotensin II generated locally from precursor angiotensin I within cardiac and vascular tissues may modulate noradrenergic transmitter release.