Abstract 13694: Greater Contribution of Endothelium-Derived Hyperpolarizing Factor to Exercise-Induced Vasodilation in African Americans Compared to Whites.
Whether impaired endothelial function in African Americans (AA) compared to Whites is due to alterations in either nitric oxide (NO) or endothelium-derived hyperpolarizing factor (EDHF) activity is unknown. We hypothesized that there is a differential racial contribution of these two factors to vasodilator tone that also influences their contribution to vasodilation during exercise.
Methods: In 46 White and 42 AA healthy subjects, we measured forearm blood flow (FBF) using strain gauge plethysmography at rest, during handgrip exercise (performed at 15%, 30% and 45% of maximum grip strength) and after sodium nitroprusside (1.6 and 3.2 μg/min) infusion. Measurements were repeated after NO blockade with L-NMMA, calcium-dependent potassium channel blockade with tetraethylammonium (TEA, inhibiting EDHF activity), and combined blockade.
Results: L-NMMA reduced resting FBF to a greater extent in Whites compared to AA (−30% vs −21%, p<0.0001), indicating decreased contribution of NO to resting tone in AA. TEA reduced resting FBF to a similar extent in AA and Whites (−17% and −15%, p<0.0001), indicating preserved contribution of EDHF in AA. Exercise-induced vasodilation was similar in Whites and AA (p=0.15). L-NMMA attenuated exercise-induced FBF to a greater extent in Whites (−21% vs. −9%, p<0.0001), indicating reduced contribution of NO in AA. TEA reduced exercise-induced vasodilation to a greater extent in AA than Whites (−20% vs −16% reduction in mean FBF, p=0.0129) indicating a greater contribution of EDHF in AA compared to Whites. Combined blockade with L-NMMA and TEA reduced exercise-induced vasodilation to a similar extent in both groups. Sodium nitroprusside-mediated dilation was greater in Whites than AA with a 22% greater mean FBF (p=0.0002), indicating reduced sensitivity of the smooth muscle cells to NO in AA.
Conclusions: Compared to Whites, healthy AA have reduced availability and sensitivity to NO at rest and during physiologic vasodilation. In contrast, EDHF activity is similar in both races at rest and it's contribution to exercise vasodilation is greater in AA compared to Whites. Increased EDHF activity compensates for reduced NO in AA, and may underlie the increased risk of hypertension and cardiovascular disease in AA.
- © 2010 by American Heart Association, Inc.