Alpha2-Adrenergic Receptor–Induced Vascular Constriction in Blacks and Whites

• Published in: Hypertension (Dallas, Tex. 1979) Tex. 1979), 2004-01, Vol.43 (1), p.31-35
• Main Authors: Muszkat, Mordechai, Sofowora, Gbenga G, Wood, Alastair J.J, Stein, C Michael
• Format: Article
• Language: English
• Subjects: Adrenergic alpha-2 Receptor Agonists; Adrenergic alpha-Agonists - pharmacology; Adult; Arterial hypertension. Arterial hypotension; Biological and medical sciences; Black or African American; Black People; Blood and lymphatic vessels; Blood vessels and receptors; Cardiology. Vascular system; Clinical manifestations. Epidemiology. Investigative techniques. Etiology; Dexmedetomidine - pharmacology; Female; Fundamental and applied biological sciences. Psychology; Hand - blood supply; Humans; Male; Medical sciences; Vasoconstriction - drug effects; Veins - drug effects; Veins - physiology; Vertebrates: cardiovascular system; White People
• ISSN: 0194-911X; 1524-4563; 1524-4563
• DOI: 10.1161/01.HYP.0000103694.30164.C7

ABSTRACT—Black Americans have a reduced hypotensive response to the α2-adrenergic receptor agonist clonidine compared with whites, despite similar central sympathoinhibition. This reduced hypotensive response might be explained by greater postsynaptic vascular α2-adrenergic receptor vasoconstrictive response. However, clonidine has a low α2/α1 selectivity ratio. Therefore, to determine the role of altered α2-adrenergic receptor vascular sensitivity in ethnic differences in vascular response, we compared local vascular responses with the highly selective α2-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 α2-adrenergic receptor–induced venoconstriction is similar in blacks and whites. These findings do not support the hypothesis that altered α2-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 α2-adrenergic receptor–mediated vascular responses