Abstract 211: Increased Blood Pressure Regulation By Nitric Oxide In Obese African American Women Unmasked By Autonomic Blockade

Abstract

African American women have the highest prevalence of hypertension (46%) in the world. African Americans (AA) have decreased vascular reactivity to pharmacologic (methacholine, nitroprusside, isoproterenol) and physiological (ischemia) stimuli. Such findings could be explained by racial differences in nitric oxide (NO) release, NO responsiveness, or by a differential suppression of NO by the sympathetic nervous system. The goal of this study was to evaluate tonic restraint of blood pressure by NO during complete autonomic blockade in obese AA vs. white women. We hypothesized that if AA women had a primary NO “deficiency” then they would have less increase in systolic blood pressure (SBP) during intravenous infusion of the NO synthase inhibitor N(ω)-monomethyl-l-arginine (L-NMMA, 250 ug/kg/min) during autonomic blockade. We studied 8 obese AA women and 9 obese white women matched by age (41±6.4 vs. 42±8.2 years, P=0.66), BMI (34±4.4 vs 35±4.1 kg/m2, P=0.83) and seated SBP (121±11 vs. 125±7 mm Hg, P=0.49). Antihypertensive medications were discontinued for 2 weeks and smokers were excluded. All subjects underwent complete autonomic blockade with the ganglionic blocker trimethaphan (TMT, 4 mg/min) followed by L-NMMA. The alpha-1 adrenergic agonist phenylephrine was titrated to clamp systolic blood pressure at 110 mm Hg prior to infusion of L-NMMA. SBP response to L-NMMA was greater in obese AA women (54±13.6 vs. 39±9.6 mm Hg in whites, P=0.02, Figure) suggesting that NO, in the absence of autonomic influences, is an important regulator of blood pressure in obese AA women. This suggests that sympathetic activation contributes to "NO deficiency" in AA.