title: Endogenous angiotensin II does not contribute to sympathetic venoconstriction in dorsal hand veins of healthy humans.
abstract: 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 microg/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.
authors.affiliation: Clinical Research Centre, University of Edinburgh, Department of Medicine, Western General Hospital, Scotland.
authors.forename: S
authors.initials: S
authors.lastname: Masumori
authors.forename: D E
authors.initials: DE
authors.lastname: Newby
authors.forename: F E
authors.initials: FE
authors.lastname: Strachan
authors.forename: N A
authors.initials: NA
authors.lastname: Boon
authors.forename: D J
authors.initials: DJ
authors.lastname: Webb
mesh_terms: D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000328:Adult; D057911:Angiotensin Receptor Antagonists; D000959:Antihypertensive Agents / Q000494:pharmacology*; D019540:Area Under Curve; D006225:Hand; D006801:Humans; D007262:Infusions, Intravenous; D019808:Losartan / Q000494:pharmacology*; D008297:Male; D009638:Norepinephrine / Q000008:administration & dosage / Q000494:pharmacology; D011945:Receptors, Angiotensin / Q000502:physiology; D012084:Renin-Angiotensin System / Q000187:drug effects / Q000502:physiology; D016037:Single-Blind Method; D014661:Vasoconstriction / Q000187:drug effects* / Q000502:physiology; D014680:Veins / Q000502:physiology*
chemical_list: D000316:Adrenergic alpha-Agonists; D057911:Angiotensin Receptor Antagonists; D000959:Antihypertensive Agents; D011945:Receptors, Angiotensin; D019808:Losartan; D009638:Norepinephrine