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Endogenous angiotensin II does not contribute to sympathetic venoconstriction in dorsal hand veins of healthy humans
Author(s) -
Masumori Satoko,
Newby David E.,
Strachan Fiona E.,
Boon Nicholas A.,
Webb David J.
Publication year - 1997
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1016/s0009-9236(97)90036-9
Subject(s) - losartan , angiotensin ii , renin–angiotensin system , vasoconstriction , medicine , norepinephrine , vasoconstrictor agents , endocrinology , receptor , blood pressure , dopamine
Background Sympathetically mediated venoconstriction is augmented by exogenously administered angiotensin II. This study was designed to assess whether endogenous angiotensin II influences sympathetically mediated venous tone. Methods Responses of dorsal hand veins to local intravenous administration of subsystemic doses of losartan, an angiotensin II type‐1 receptor antagonist, were assessed with use of a well‐validated displacement 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 venoconstriction produced by a single deep breath were compared in the presence of either saline placebo or 30 μg/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 venoconstriction. 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 venoconstriction in healthy humans. However, endogenous angiotensin II may have a role in circumstances of renin‐angiotensin system activation, such as salt depletion. Clinical Pharmacology & Therapeutics (1997) 62 , 327–333; doi: