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Research Article Free access | 10.1172/JCI116347

Homologous upregulation of human arterial alpha-adrenergic responses by guanadrel.

R V Hogikyan and M A Supiano

Department of Internal Medicine, University of Michigan, Ann Arbor.

Find articles by Hogikyan, R. in: PubMed | Google Scholar

Department of Internal Medicine, University of Michigan, Ann Arbor.

Find articles by Supiano, M. in: PubMed | Google Scholar

Published April 1, 1993 - More info

Published in Volume 91, Issue 4 on April 1, 1993
J Clin Invest. 1993;91(4):1429–1435. https://doi.org/10.1172/JCI116347.
© 1993 The American Society for Clinical Investigation
Published April 1, 1993 - Version history
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Abstract

The purpose of this study was to test the hypothesis that there is homologous upregulation of arterial alpha-adrenergic responsiveness during suppression of sympathetic nervous system (SNS) activity in humans. 10 subjects (19-28 yr) were studied during placebo and when SNS activity was suppressed by guanadrel. Changes in forearm blood flow (FABF) mediated by the intraarterial infusion of norepinephrine (NE), angiotensin II (AII), and phentolamine were measured by plethysmography. During guanadrel compared with placebo, plasma NE levels (1.28 +/- 0.09-0.85 +/- 0.06 nM; P = 0.0001) and the extra vascular NE release rate derived from [3H]NE kinetics were lower (7.1 +/- 0.7-4.0 +/- 0.2 nmol/min per m2; P = 0.0004), suggesting suppression of SNS activity. During guanadrel, there was increased sensitivity in the FABF response to NE (analysis of variance P = 0.03). In contrast, there was no difference in the FABF response to AII (analysis of variance P = 0.81), suggesting that the upregulation observed to NE was homologous. The increase in FABF during phentolamine was similar during guanadrel compared with placebo (guanadrel: 141 +/- 37 vs. placebo; 187 +/- 27% increase; P = 0.33), suggesting that there was at least partial compensation to maintain constant endogenous arterial alpha-adrenergic tone. We conclude that there is homologous upregulation of arterial alpha-adrenergic responsiveness in humans when SNS activity is suppressed by guanadrel.

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