ENDOGENOUS ANGIOTENSIN-II DOES NOT CONTRIBUTE TO SYMPATHETIC VENOCONSTRICTION IN DORSAL HAND VEINS OF HEALTHY HUMANS

Background: Sympathetically mediated venoconstriction is augmented by exogenously administered angiotensin II. This study was designed to as sess whether endogenous angiotensin II influences sympathetically medi ated venous tone. Methods: Responses of dorsal hand veins to local int ravenous administration of subsystemic doses of losartan, an angiotens in II type-1 receptor antagonist, were assessed with use of a well-val idated displace ment technique in eight healthy male volunteers. In a four-phase study, responses to local infusions of angiotensin II (4 to 64 ng/min) and norepinephrine (1 to 128 ng/min) or to sympathetic ven oconstriction produced by a single deep breath were compared in the pr esence of either saline placebo or 30 mu g/min losartan. Each phase of the study was conducted on a separate day, in random order, and each phase was separated by at least 1 week. Results: Angiotensin II (p = 0 .03) and norepinephrine (p < 0.001) caused dose-dependent venoconstric tion. Losartan attenuated the venoconstriction induced by angiotensin II (p = 0.048) but had no effect on the responses to norepinephrine or the venoconstriction induced by a single deep breath. Conclusions: In contrast to exogenously administered angiotensin II, basal endogenous angiotensin II does not influence sympathetically mediated venoconstr iction in healthy humans. However, endogenous angiotensin II may have a role in circumstances of renin-angiotensin system activation, such a s salt depletion.