Evidence for prejunctional inhibition of norepinephrine release by captopril in spontaneously hypertensive rats

Pretreatment of spontaneously hypertensive rats (SHR) with the converting enzyme inhibitor captopril (10 or 100 mg/kg p.o.) had no effect on pressor responses to angiotensin II or norepinephrine whereas the response to angiotensin I was markedly inhibited. In contrast, pressor responses to sympathet...

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Bibliographic Details
Published inEuropean journal of pharmacology Vol. 68; no. 2; p. 209
Main Authors Antonaccio, M J, Kerwin, L
Format Journal Article
LanguageEnglish
Published Netherlands 01.01.1980
Subjects
Angiotensin II - biosynthesis
Animals
Blood Pressure - drug effects
Captopril - pharmacology
Heart Rate - drug effects
Hypertension - physiopathology
Norepinephrine - metabolism
Proline - analogs & derivatives
Rats
Sympathetic Nervous System - drug effects
Sympathetic Nervous System - physiology
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Summary:Pretreatment of spontaneously hypertensive rats (SHR) with the converting enzyme inhibitor captopril (10 or 100 mg/kg p.o.) had no effect on pressor responses to angiotensin II or norepinephrine whereas the response to angiotensin I was markedly inhibited. In contrast, pressor responses to sympathetic stimulation in pithed SHR were inhibited by captopril whereas the positive chronotropic responses to stimulation were unaltered. These results suggest that captopril causes a prejunctional inhibition of norepinephrine release to sympathetic nerve stimulation which is selective for the vasculature. This is probably due to inhibition of angiotensin II formation in the vasculature.
ISSN:0014-2999
DOI:10.1016/0014-2999(80)90325-8