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Vasopressin-mediated forearm vasodilation in normal humans. Evidence for a vascular vasopressin V2 receptor.

Publication ,  Journal Article
Hirsch, AT; Dzau, VJ; Majzoub, JA; Creager, MA
Published in: J Clin Invest
August 1989

Arginine vasopressin (AVP) is a potent vasopressor and antidiuretic neurohormone. However, when administered intravenously to humans, AVP causes forearm vasodilation. This effect has been attributed to sympathetic withdrawal, secondary to AVP-induced sensitization of baroreceptors. The possibility that AVP also causes forearm vasodilation directly has not been examined. Accordingly, the direct effect of AVP was determined by studying the forearm blood flow (FBF) response to intraarterial (IA) AVP infusion (0.01-1.0 ng/kg per min). Infusion of IA AVP increased FBF (96%) in the infused arm, but not the control arm, in a dose-dependent manner. The role of specific AVP V1 receptors in mediating this FBF response was determined before and after pretreatment with a V1 antagonist (AVP-A). AVP-A alone had no effect on FBF, but coadministration of AVP and AVP-A potentiated the vasodilatory response (223%). IA infusion of the V2 agonist, 1-desamino[8-D-arginine] vasopressin, caused a dose-dependent increase in FBF. These findings suggest that AVP causes direct, dose-dependent vasodilation in the human forearm that may be mediated by V2 vasopressinergic receptors. In contrast, AVP infusion caused digital vasoconstriction that was blocked by AVP-A, whereas dDAVP did not affect digital blood flow. Thus, AVP induces regionally selective vascular effects, with concurrent forearm vasodilation and digital vasoconstriction.

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Published In

J Clin Invest

DOI

ISSN

0021-9738

Publication Date

August 1989

Volume

84

Issue

2

Start / End Page

418 / 426

Location

United States

Related Subject Headings

  • Vasodilation
  • Receptors, Vasopressin
  • Receptors, Angiotensin
  • Prostaglandins
  • Male
  • Immunology
  • Humans
  • Hemodynamics
  • Forearm
  • Female
 

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APA
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Hirsch, A. T., Dzau, V. J., Majzoub, J. A., & Creager, M. A. (1989). Vasopressin-mediated forearm vasodilation in normal humans. Evidence for a vascular vasopressin V2 receptor. J Clin Invest, 84(2), 418–426. https://doi.org/10.1172/JCI114182
Hirsch, A. T., V. J. Dzau, J. A. Majzoub, and M. A. Creager. “Vasopressin-mediated forearm vasodilation in normal humans. Evidence for a vascular vasopressin V2 receptor.J Clin Invest 84, no. 2 (August 1989): 418–26. https://doi.org/10.1172/JCI114182.
Hirsch AT, Dzau VJ, Majzoub JA, Creager MA. Vasopressin-mediated forearm vasodilation in normal humans. Evidence for a vascular vasopressin V2 receptor. J Clin Invest. 1989 Aug;84(2):418–26.
Hirsch, A. T., et al. “Vasopressin-mediated forearm vasodilation in normal humans. Evidence for a vascular vasopressin V2 receptor.J Clin Invest, vol. 84, no. 2, Aug. 1989, pp. 418–26. Pubmed, doi:10.1172/JCI114182.
Hirsch AT, Dzau VJ, Majzoub JA, Creager MA. Vasopressin-mediated forearm vasodilation in normal humans. Evidence for a vascular vasopressin V2 receptor. J Clin Invest. 1989 Aug;84(2):418–426.

Published In

J Clin Invest

DOI

ISSN

0021-9738

Publication Date

August 1989

Volume

84

Issue

2

Start / End Page

418 / 426

Location

United States

Related Subject Headings

  • Vasodilation
  • Receptors, Vasopressin
  • Receptors, Angiotensin
  • Prostaglandins
  • Male
  • Immunology
  • Humans
  • Hemodynamics
  • Forearm
  • Female