(Hypertension. 1997;30:918-921.)
© 1997 American Heart Association, Inc.
Articles |
Decreased Vasodilator Response to Isoproterenol During Nitric Oxide Inhibition in Humans
From the Cardiology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Md.
Correspondence to Dr Julio A. Panza, Cardiology Branch, National Institutes of Health, Bldg 10, Room 7B-15, Bethesda, MD 20892-1650. E-mail panzaj{at}gwgate.nhlbi.nih.gov
Abstract The vasodilator effect of ß-adrenergic agonists has traditionally been ascribed solely to a direct effect on vascular smooth muscle. Experimental studies, however, have suggested a role of endothelium-derived nitric oxide (NO) in ß-adrenergic–mediated vasodilation. The purpose of this investigation was to determine whether NO contributes to the vasodilator effect of ß-adrenergic stimulation in humans. We analyzed the forearm blood flow response to increasing doses of isoproterenol (50, 100, and 200 ng/min), a ß-adrenoceptor agonist, during the concomitant infusion of saline or NG-monomethyl-L-arginine (L-NMMA; 4 µmol/min), a blocker of NO synthesis, in 23 normal subjects (9 men and 14 women, aged 48±7 years). The effect of L-NMMA was also assessed during infusion of sodium nitroprusside (0.8, 1.6, and 3.2 µg/min), an exogenous NO donor. Drugs were infused into the brachial artery, and forearm blood flow was measured by plethysmography. The vasodilator effect of isoproterenol was significantly blunted during the administration of L-NMMA compared with saline (maximum flow, 7.7±4 versus 11.2±5 mL · min-1 · dL-1, respectively; P<.001). In contrast, the vasodilator response to sodium nitroprusside was not significantly affected by the infusion of L-NMMA (maximum flow, 8.8±3.7 mL · min-1 · dL-1 during L-NMMA versus 8.9±3.2 mL · min-1 · dL-1 during saline; P=.25). These findings indicate that NO inhibition blunts the vasodilator effect of ß-adrenergic agonists in the human forearm and suggest that an abnormal response to adrenergic stimulation may occur in conditions associated with impaired NO activity.
Key Words: ß-adrenergic receptors • vasodilation • nitric oxide • endothelium • isoproterenol
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