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The effect of enalapril on baroreceptor mediated reflex function in normotensive subjects.
Author(s) -
Giudicelli JF,
Berdeaux A.,
Edouard A.,
Richer C.,
Jacolot D.
Publication year - 1985
Publication title -
british journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.216
H-Index - 146
eISSN - 1365-2125
pISSN - 0306-5251
DOI - 10.1111/j.1365-2125.1985.tb05063.x
Subject(s) - enalapril , baroreflex , baroreceptor , blood pressure , phenylephrine , aldosterone , plasma renin activity , medicine , heart rate , endocrinology , reflex , renin–angiotensin system , anesthesia , chemistry , angiotensin converting enzyme
The effects of enalapril, 20 mg orally, on the responses to baroreflex activation and deactivation by respectively phenylephrine and nitroglycerin were investigated in normotensive subjects on a normal sodium diet, with simultaneous measurement of plasma renin activity (PRA), converting enzyme activity (PCEA), aldosterone and catecholamines. Enalapril, 4 h after administration, lowered artificial blood pressure without modifying heart rate and plasma catecholamines. PCEA was abolished, PRA increased and plasma aldosterone decreased. Enalapril (a) displaced to the left the baroreflex set‐point, (b) did not affect baroreflex sensitivity since the slopes of the RR‐ interval/systolic blood pressure regression lines remained unchanged during both activation and deactivation and (c) did not modify baroreflex efficacy since the maximal RR‐interval responses as well as the overall RR‐interval‐time products to identical blood pressure variations were not modified. Thus, enalapril induced a resetting of the baroreflex, which probably accounts for the lack of reflex tachycardia observed during the drug‐induced fall in blood pressure.