Decreased vasodilator response to isoproterenol during nitric oxide inhibition in humans
Decreased vasodilator response to isoproterenol during nitric oxide inhibition in humans
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DOI：
10.1161/01.hyp.30.4.918
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发表时间：
1997-10-01
期刊：
影响因子：
8.3
通讯作者：
Panza, JA
中科院分区：
文献类型：
--
作者：
Cardillo, C;Kilcoyne, CM;Panza, JA
β-肾上腺素能激动剂的血管舒张作用传统上仅归因于对血管平滑肌的直接作用。然而，实验研究表明内皮源性一氧化氮 (NO) 在 β-肾上腺素能介导的血管舒张中发挥作用。本研究的目的是确定 NO 是否有助于人体 β-肾上腺素能刺激的血管舒张作用。我们分析了 23 名正常受试者（9 名男性和 14 名女性，老年）在同时输注盐水或 N-G-单甲基-L-精氨酸（L-NMMA；4 μmol/min）（一种 NO 合成阻滞剂）期间，对增加剂量的异丙肾上腺素（50、100 和 200 ng/min）（一种 β-肾上腺素受体激动剂）的前臂血流反应。 48+/-7 岁）。还在输注硝普钠（0.8、1.6 和 3.2 μg/min）（一种外源性 NO 供体）期间评估了 L-NMMA 的作用。将药物注入肱动脉，并通过体积描记法测量前臂血流量。与生理盐水相比，L-NMMA 给药期间异丙肾上腺素的血管舒张作用显着减弱（最大流量分别为 7.7+/-4 与 11.2+/-5 mL . min(-1) . dL(-1)；P
The vasodilator effect of beta-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 beta-adrenergic-mediated vasodilation. The purpose of this investigation was to determine whether NO contributes to the vasodilator effect of beta-adrenergic stimulation in humans. We analyzed the forearm blood flow response to increasing doses of isoproterenol (50, 100, and 200 ng/min), a beta-adrenoceptor agonist, during the concomitant infusion of saline or N-G-monomethyl-L-arginine (L-NMMA; 4 mu mol/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 mu g/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