title: Sympathomoderating influence of benazepril in essential hypertension.
abstract: OBJECTIVE
  In essential hypertension, captopril attenuates forearm vasoconstriction reflexly induced by deactivation of cardiopulmonary and arterial baroreceptors, thus exerting a sympathomoderating effect. We investigated whether this is a common effect of angiotensin converting enzyme (ACE) inhibitors.
  
  
  METHODS
  Cardiopulmonary and arterial baroreceptors were deactivated by progressively reducing central venous pressure (CVP) through progressively greater lower body negative pressures in eight untreated mild essential hypertensives on a moderately low-sodium diet (50 mmol/l per day). This deactivation was performed after oral administration of the non-sulphidrylic ACE inhibitor benazepril (10 mg) and placebo according to a double-blind randomized crossover experimental design.
  
  
  RESULTS
  After placebo, the reduction in CVP increased forearm vascular resistance (FVR; mean arterial pressure: plethysmographic forearm blood flow ratio). After benazepril, baseline blood pressure (beat-to-beat finger pressure) and FVR were significantly reduced whilst plasma angiotensin II was suppressed and PRA increased (both measured by radioimmunoassay). The FVR increases induced by progressive CVP reduction were less than after placebo administration, and the overall difference was statistically significant. Benazepril did not affect the reflex FVR reduction observed by increasing CVP through leg raising, nor the reflex changes in plasma norepinephrine measured by high-performance liquid chromatography accompanying the changes in FVR.
  
  
  CONCLUSIONS
  Benazepril attenuates sympathetic vasoconstriction as does captopril. This effect (which is mainly operative during an increased sympathetic drive and exerted through a reduction of adrenoceptor responsiveness) is thus likely to be a class- rather than a compound-related feature.
authors.affiliation: Cattedra di Medicina Interna, Università di Milano, Italy.
authors.forename: C
authors.initials: C
authors.lastname: Giannattasio
authors.forename: B M
authors.initials: BM
authors.lastname: Cattaneo
authors.forename: S
authors.initials: S
authors.lastname: Omboni
authors.forename: G
authors.initials: G
authors.lastname: Seravalle
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: Morganti
authors.forename: G
authors.initials: G
authors.lastname: Grassi
authors.forename: A
authors.initials: A
authors.lastname: Zanchetti
authors.forename: G
authors.initials: G
authors.lastname: Mancia
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D001552:Benzazepines / Q000627:therapeutic use*; D004039:Diet, Sodium-Restricted; D004311:Double-Blind Method; D005260:Female; D006801:Humans; D006973:Hypertension / Q000188:drug therapy*; D008150:Lower Body Negative Pressure; D008297:Male; D008875:Middle Aged; D009638:Norepinephrine / Q000097:blood; D011311:Pressoreceptors / Q000187:drug effects; D012084:Renin-Angiotensin System / Q000187:drug effects; D013564:Sympathetic Nervous System / Q000187:drug effects*; D014655:Vascular Resistance / Q000187:drug effects; D014661:Vasoconstriction / Q000187:drug effects*
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D001552:Benzazepines; C044946:benazepril; D009638:Norepinephrine