Published online before print December 1, 2003, doi: 10.1161/01.HYP.0000103694.30164.C7
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(Hypertension. 2004;43:31.)
© 2004 American Heart Association, Inc.
Scientific Contributions |
Alpha2-Adrenergic Receptor–Induced Vascular Constriction in Blacks and Whites
From the Division of Clinical Pharmacology, Vanderbilt University School of Medicine, Nashville, Tenn.
Correspondence to C. Michael Stein, MD, Division of Clinical Pharmacology, 560 RRB, Vanderbilt University School of Medicine, Nashville, TN 37232-6602. E-mail michael.stein{at}vanderbilt.edu
Black Americans have a reduced hypotensive response to the 
2-adrenergic receptor agonist clonidine compared with whites, despite similar central sympathoinhibition. This reduced hypotensive response might be explained by greater postsynaptic vascular 2-adrenergic receptor vasoconstrictive response. However, clonidine has a low 2/1 selectivity ratio. Therefore, to determine the role of altered 2-adrenergic receptor vascular sensitivity in ethnic differences in vascular response, we compared local vascular responses with the highly selective 2-adrenergic receptor agonist dexmedetomidine in healthy black (n=18) and white (n=19) subjects. Increasing doses of dexmedetomidine (0.001 to 1000 ng/min) were infused into a dorsal hand vein, and the local response was measured with a linear variable differential transformer. Dexmedetomidine caused pronounced venoconstriction, with an average (±SD) maximum response of 74.5±17.72% but with no difference between blacks and whites. There was substantial intersubject variability in the sensitivity to dexmedetomidine; the dose resulting in 50% (ED50) of maximum vasoconstriction ranged from 0.08 ng/min to 256 ng/min. The geometric mean ED50 was 2.28 ng/min (95% CI, 0.02 to 271.6 ng/min) in blacks and 1.58 ng/min (95% CI, 0.11 to 24.55 ng/min) in whites (P=0.59). Our data indicate that 2-adrenergic receptor–induced venoconstriction is similar in blacks and whites. These findings do not support the hypothesis that altered 2-adrenergic receptor sensitivity is the explanation for the decreased blood pressure response to systemic administration of clonidine in blacks. The response to dexmedetomidine provides a model that will allow further study of the regulation of 2-adrenergic receptor–mediated vascular responses
Key Words: adrenergic receptor agonists • ethnicity • human • receptors, adrenergic, alpha • vasoconstriction • veins
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