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Sensitization of human α 1 ‐ and α 2 ‐adrenergic venous responses by guanadrel sulfate
Author(s) -
Sekkarie Mohamed A,
Egan Brent M,
Neubig Richard R,
Supiano Mark A
Publication year - 1990
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 - 10.1038/clpt.1990.190
Subject(s) - clonidine , phenylephrine , prazosin , adrenergic agonist , norepinephrine , medicine , sensitization , anesthesia , adrenergic , rauwolscine , endocrinology , antagonist , receptor , blood pressure , dopamine , immunology
The α 1 ‐ and α 2 ‐adrenergic venoconstriction in dorsal hand veins of normal subjects was determined by infusion of phenylephrine or clonidine. Oral administration of prazosin reduced the constriction response to phenylephrine but not to clonidine. Subjects were treated for 3 weeks in a randomized crossover design with placebo or guanadrel sulfate. Guanadrel reduced sympathetic tone (i.e., plasma norepinephrine and norepinephrine release rate), whereas venous responses to phenylephrine and clonidine were both augmented during guanadrel treatment. The effect on phenylephrine responses was primarily attributable to a decrease in the median effective concentration with a small increase in maximum response. Clonidine showed a markedly increased maximum response with a small increase in the median effective concentration. Platelet α 2 ‐adrenergic receptors increased slightly but there was no change in the amount of platelet pertussis toxin substrate during guanadrel treatment. Thus reduction in sympathetic tone in normal young men results in increased venous responses to both α 1 ‐ and α 2 ‐agonists. Clinical Pharmacology and Therapeutics (1990) 48, 537–543; doi: 10.1038/clpt.1990.190