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Published on: June 3, 2019
Autonomic Blockade Reverses Endothelial Dysfunction in Obesity-Associated Hypertension
Alfredo Gamboa1, Rocío Figueroa2, Sachin Y Paranjape2
1From the Division of Clinical Pharmacology (A.G., R.F., S.Y.P., G.F., A.D., I.B.), Departments of Medicine (A.G., R.F., S.Y.P., G.F., A.D., I.B.), and Pharmacology (I.B.), Vanderbilt University, Nashville, TN. alfredo.gamboa@vanderbilt.edu.
Abstract:
Impaired nitric oxide (NO) vasodilation (endothelial dysfunction) is associated with obesity and thought to be a factor in the development of hypertension. We previously found that NO synthesis inhibition had similar pressor effects in obese hypertensives compared with healthy control during autonomic blockade, suggesting that impaired NO vasodilation is secondary to sympathetic activation. We tested this hypothesis by determining the effect of autonomic blockade (trimethaphan 4 mg/min IV) on NO-mediated vasodilation (increase in forearm blood flow to intrabrachial acetylcholine) compared with endothelial-independent vasodilation (intrabrachial sodium nitroprusside) in obese hypertensive subjects (30
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