title: Reflex control of circulation and angiotensin converting enzyme inhibition in man.
abstract: Removal of the facilitating effect of angiotensin II on sympathetic cardiovascular influences may enhance the antihypertensive effect of angiotensin converting enzyme (ACE) inhibitors but may also disturb reflexes involved in blood pressure homeostasis. To test this hypothesis in essential hypertensive subjects, the forearm vasomotor response to cardiopulmonary receptor deactivation (lower body negative pressure) was studied before and after acute or prolonged administration of captopril at doses capable of lowering blood pressure and blocking the formation of angiotensin II. After either acute or prolonged captopril administration there was less response (i.e. forearm vasoconstriction) than in the no-drug state. However, in the same subjects, another reflex response to cardiopulmonary receptor deactivation, the increase in plasma renin activity, was not blunted by the drug. Furthermore, the other major reflex responsible for blood pressure homeostasis, the arterial baroreflex, was left unchanged or was even favoured by administration of clinically effective doses of captopril. This finding applied to both the heart rate and the blood pressure modulating ability of the reflex (vasoactive drug and neck chamber techniques, respectively). Thus, reflex control of circulation may be adversely affected by ACE inhibition. However, this does not include all reflex targets and at least one major reflex is preserved following this pharmacological intervention. This may explain why our patients showed no orthostatic hypotension during chronic treatment with ACE inhibitors.
authors.affiliation: Cattedra di Semeiotica Medica e Istituto di Clinica Medica, Università di Milano, Italy.
authors.forename: G
authors.initials: G
authors.lastname: Mancia
authors.forename: C
authors.initials: C
authors.lastname: Giannattasio
authors.forename: G
authors.initials: G
authors.lastname: Grassi
authors.forename: A
authors.initials: A
authors.lastname: Morganti
authors.forename: A
authors.initials: A
authors.lastname: Zanchetti
mesh_terms: D001794:Blood Pressure / Q000187:drug effects; D002216:Captopril / Q000494:pharmacology*; D002346:Carotid Sinus / Q000187:drug effects / Q000503:physiopathology; D002496:Central Venous Pressure / Q000187:drug effects; D005542:Forearm / Q000098:blood supply; D006321:Heart / Q000294:innervation; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000503:physiopathology*; D008150:Lower Body Negative Pressure; D008168:Lung / Q000294:innervation; D009638:Norepinephrine / Q000097:blood; D011311:Pressoreceptors / Q000187:drug effects / Q000503:physiopathology*; D012018:Reflex / Q000187:drug effects*; D012039:Regional Blood Flow / Q000187:drug effects; D012084:Renin-Angiotensin System; D014655:Vascular Resistance / Q000187:drug effects
chemical_list: D002216:Captopril; D009638:Norepinephrine