ARTICLE: PDF OnlyMoursi Mahmoud; El-Dakhakhny, Mohamed; Scholkens, Bernward A.; Unger, ThomasJournal of Cardiovascular Pharmacology: 1987 - p 125-128 Free Abstract Summary The interaction of the converting enzyme inhibitor (CFI) ramipril with sympathetic neurotransmission and the baroreceptor reflex (BRR) was investigated in conscious stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive Wistar–Kyoto (WKY) controls. Intravenous (i.v.( injection of ramipril (100 μg) attenuated the pressor responses to i.v. noradrenaline (NA) in SHRSP and WKY rats. Ganglionic blockade was performed with pentolinium (10 mg/kg i.v.), and blood pressure (BP) was subsequently supported with i.v. NA (1 μg/min). angiotensin II TANG II. 500 ng/min), or NA plus a suppressor dose (0.1 ng/min) of ANG II. Intravenous injection of ramiprilat (100 μg) significantly de-creased NA-supported BP in SHRSP and WKY rats for more than 30 min, hut did not lower BP in rats supported with ANG II or with NA plus a suppressor dose of ANG II. In SHRSP and WKY rats pretreated intracerebroventricularly (i.c.v.) with ramiprilat (0.5 μg/min for 30 min). the slope of the BRR curve between increases in systolic BP and prolongation in pulse interval following bolus i.v. injections of methoxamine (10–100 μg/kg) was steeper than in vehicle-pretreated controls. In contrast, i.v. pre-treatment with the same dose of the CEI did not increase BRR sensitivity. Our data in conscious animals demonstrate that CEI can interfere acutely with the autonomic nervous system through postsynaptic inhibition of neurotransmission and sensitization of the baroreceptor reflex. The relevance of this mechanism for the chronic antihypertensive actions of CEI remains to he established. Copyright © 1987 Wolters Kluwer Health, Inc. All rights reserved.