title: Effect of angiotensin converting enzyme inhibition on cardiovascular regulation during reflex sympathetic activation in sodium-replete patients with essential hypertension.
abstract: In order to investigate whether angiotensin II (Ang II) may contribute to cardiovascular regulation through facilitation of the adrenergic function, we examined the haemodynamic and humoral effects of the application of lower-body negative pressure (LBNP) in sodium-replete patients with essential hypertension before and after acute and chronic angiotensin converting enzyme (ACE) inhibition. We measured the changes in blood pressure, heart rate, central venous pressure, forearm blood flow, plasma noradrenaline, renin activity and Ang II induced by LBNP of two different magnitudes: a milder one deactivating predominantly the cardiopulmonary receptors (mild LBNP), and a greater one deactivating both the cardiopulmonary and the arterial baroreceptors (strong LBNP). We found that during mild LBNP systemic blood pressure was maintained after acute and chronic ACE inhibition, as in control studies; however, the decrements in forearm blood flow and the increments in forearm vascular resistance caused by LBNP were diminished after ACE inhibition (the latter by 69 and 67%, respectively, in acute and chronic studies), in spite of the fact that the falls in central venous pressure and the increases in noradrenaline (NA) were similar to those observed in control conditions. During strong LBNP, the fall in systemic blood pressure was greater after acute and chronic ACE inhibition than in control conditions and was associated with a reduction in the response of forearm vascular resistance similar to that observed during mild LBNP, while the increments in NA were again superimposable to those seen before ACE inhibition. These alterations in the haemodynamic responses to LBNP induced by ACE inhibition were associated with significant increments in basal plasma renin activity and with marked reductions in Ang II. These findings suggest that even in the sodium-replete state, Ang II exerts a facilitatory action on adrenergic function that is physiologically relevant for the regulation of forearm blood flow and the maintenance of blood pressure during the application of gravitational stresses.
authors.affiliation: Istituto di Clinica Medica Generale e Terapia Medica, Università di Milano, Italy.
authors.forename: A
authors.initials: A
authors.lastname: Morganti
authors.forename: G
authors.initials: G
authors.lastname: Grassi
authors.forename: C
authors.initials: C
authors.lastname: Giannattasio
authors.forename: G
authors.initials: G
authors.lastname: Bolla
authors.forename: L
authors.initials: L
authors.lastname: Turolo
authors.forename: A
authors.initials: A
authors.lastname: Saino
authors.forename: C
authors.initials: C
authors.lastname: Sala
authors.forename: G
authors.initials: G
authors.lastname: Mancia
authors.forename: A
authors.initials: A
authors.lastname: Zanchetti
mesh_terms: D000328:Adult; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D002216:Captopril / Q000627:therapeutic use*; D002319:Cardiovascular System / Q000503:physiopathology*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D011311:Pressoreceptors / Q000503:physiopathology; D012964:Sodium / Q000378:metabolism; D013564:Sympathetic Nervous System / Q000503:physiopathology*
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D002216:Captopril; D012964:Sodium