title: Angiotensin converting enzyme inhibition. Systemic and regional hemodynamics in rats and humans.
abstract: The systemic and regional hemodynamic effects of angiotensin I converting enzyme inhibitors (ACEIs) have been investigated using different experimental methods (pulsed Doppler, radioactive microspheres), either in rats (normotensive NT or genetically hypertensive SHRs) or in humans (healthy volunteers or patients with congestive heart failure CHF). All ACEIs decreased systemic vascular resistance but the profile of their peripheral vasodilating properties was heterogeneous. ACEI-induced vasodilation primarily affected the kidney in rats and in humans and this effect was accompanied by a strong and consistent increase in renal blood flow. This occurred even at non-hypotensive doses in SHRs and CHF patients and resulted in a favorable redistribution of cardiac output towards the kidney. In the muscular vascular bed, ACEIs also decreased local vascular resistance in rats and in humans, whether normotensive or hypertensive. In humans, this vasodilation affected both the arterioles and the large conductance vessels, more markedly in CHF patients than in normotensive subjects. Muscular blood flow was increased and a favorable redistribution of cardiac output towards the muscle occurred. Cerebral blood flow in SHRs and carotid blood flow in humans were augmented, whereas hepatosplanchnic blood flow was increased in rats but not modified in humans. There was no major difference between the regional vasodilating profiles of the different ACEIs, but captopril was somewhat less active at the muscular level. In conclusion, ACEI-induced regional vasodilation is heterogeneous, preferentially affecting the kidney and the muscle. In the latter, both arterioles and large conductance vessels are dilated.
authors.affiliation: Département de Pharmacologie, Faculté de Médecine Paris-Suc, Le Kremlin-Bicêtre, France.
authors.forename: J F
authors.initials: JF
authors.lastname: Giudicelli
authors.forename: C
authors.initials: C
authors.lastname: Richer
authors.forename: C
authors.initials: C
authors.lastname: Richard
authors.forename: C
authors.initials: C
authors.lastname: Thuillez
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D000818:Animals; D002302:Cardiac Output / Q000187:drug effects; D006333:Heart Failure / Q000188:drug therapy / Q000503:physiopathology; D006439:Hemodynamics / Q000187:drug effects* / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000503:physiopathology; D007211:Indoles / Q000494:pharmacology*; D008297:Male; D020913:Perindopril; D051381:Rats; D011918:Rats, Inbred SHR; D011919:Rats, Inbred Strains; D012039:Regional Blood Flow / Q000187:drug effects; D014655:Vascular Resistance / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D007211:Indoles; D020913:Perindopril