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Impaired endothelial‐dependent forearm vascular relaxation in black Americans
Author(s) -
Jones Drew S.,
Andrawis Nabil S.,
Abernethy Darrell R.
Publication year - 1999
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 - 10.1016/s0009-9236(99)70135-9
Subject(s) - medicine , brachial artery , sodium nitroprusside , forearm , vascular resistance , population , cardiology , vasodilation , plethysmograph , endocrinology , blood pressure , surgery , nitric oxide , environmental health
Background Hypertension is a major cause of morbidity and mortality in the general population and has an even more significant impact on the black community in particular. Explaining the interethnic differences has been difficult. Differences in endothelial function may provide some insight into the causes of the increased incidence of hypertension in the black population versus their white cohorts. Methods In this study 16 black subjects and 12 white subjects received brachial artery infusions of acetylcholine (12.5, 25, and 50 μg/min) and angiotensin II (3.82, 9.55, and 19.10 ng/min). Measurement of forearm vascular resistance by venous occlusion plethysmography was conducted. Results The dose of acetylcholine at 50% maximal observed response (EC 50 ) for black subjects was 10.6 ± 2.39 μg/min and 3.3 ± 0.44 μg/min in the white subjects (mean ± SEM; P < .05). Sodium nitroprusside infusions at 1 and 2 μg/min did not cause a significant difference in response between the 2 groups. After angiotensin II was infused, forearm vascular resistance E max was 3.42 ± 0.78 mm Hg/100 mL tissue volume/min for black subjects and 3.16 ± 0.99 mm Hg/100 mL tissue volume/min for white subjects. Conclusion This study shows impaired endothelial‐dependent forearm vascular relaxation as measured by decreased acetylcholine response in black subjects. This impairment in endothelial function may contribute to the increased incidence of hypertension in black subjects compared with white subjects. Mechanisms for this finding warrant further investigation. Clinical Pharmacology & Therapeutics (1999) 65 , 408–412; doi: