Abstract 403: Autonomic Blockade Improves “Endothelial Dysfunction” in Obesity-Associated Hypertensive Human Subjects

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Nitric oxide (NO) deficiency (“endothelial dysfunction”) is a hallmark of obesity and is thought to contribute to hypertension. In a previous study, however, we did not find differences in NO function between hypertensive and normotensive subjects if autonomic activity was removed with ganglionic blockade. We hypothesized, therefore, that sympathetic activation, known to occur in obesity hypertension, contributes to NO mediated endothelial dysfunction. To test this hypothesis we determined NO-mediated vasodilation (increase in forearm blood flow, FBF, to intrabrachial acetylcholine, ACh) and endothelial independent vasodilation (intrabrachial sodium nitroprusside, SNP) in obese hypertensive subjects (30

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