Vasodilation in black Americans: Attenuated nitric oxide-mediated responses*
- 9 October 1997
- journal article
- Published by Wiley in Clinical Pharmacology & Therapeutics
- Vol. 62 (4) , 436-443
- https://doi.org/10.1016/s0009-9236(97)90122-3
Abstract
Background Attenuated vasodilation in response to the intra‐arterial administration of the β‐adrenergic agonist isoproterenol (INN, isoprenaline), an endothelium‐independent vasodilator, has previously been observed in normotensive black Americans. To determine whether this reflected a more generalized attenuation of responses to vasodilators, we compared forearm blood flow responses to the endothelium‐dependent vasodilator methacholine and the endothelium‐independent vasodilator sodium nitroprusside in young normotensive black men and white men. Methods Forearm blood flow responses to the intra‐arterial administration of isoproterenol (10 to 400 ng/min), methacholine (0.25 to 8 μg/min), and sodium nitroprusside (0.25 to 8 μg/min) were measured with use of venous occlusion plethysmography in 11 normotensive black men (mean ± SE age, 30.5 ± 2.2 years) and nine normotensive white men (mean age, 28.0 ± 3.2 years). Results Baseline characteristics, including baseline forearm blood flow, were similar in the black and the white subjects. Vasodilation in response to isoproterenol, sodium nitroprusside, and methacholine was significantly attenuated in black subjects, resulting respectively in a 3.7‐fold, 3.6‐fold, and 5.0‐fold increase in forearm blood flow in black subjects and a 7.5‐fold, 5.2‐fold, and 6.9‐fold increase in forearm blood flow in white subjects (ANOVA; isoproterenol, p < 0.0001; sodium nitroprusside, p < 0.0001; methacholine, p = 0.01). Conclusions Our finding of attenuated nitric oxide‐mediated vasodilation in response to methacholine and sodium nitroprusside in healthy black American men suggests that attenuated vasodilation in black subjects is a relatively generalized phenomenon, resulting in attenuated responses to multiple vasodilators that act through different receptor‐ and nonreceptor‐mediated mechanisms. Clinical Pharmacology & Therapeutics (1997) 62, 436–443; doi:Keywords
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