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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Adrenergic alpha-1 Receptor Agonists, Adrenergic alpha-2 Receptor Agonists, Adrenergic alpha-Agonists, Adult, Brachial Artery, Clonidine, Dose-Response Relationship, Drug, Drug Interactions, Endothelium, Vascular, Enzyme Inhibitors, Forearm, Humans, Male, Methoxamine, Nitric Oxide, Nitric Oxide Donors, Nitric Oxide Synthase, Norepinephrine, Regional Blood Flow, Research Design, Vasodilation, Vasodilator Agents, omega-N-Methylarginine.
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Is endothelium-dependent NO-mediated vasodilation in humans attenuated by peripheral alpa1-adrenoceptor activation? Context: The release of nitric oxide is controlled by cholinergic and adrenergic receptors. Recent observations suggest that activation of alpha-adrenoceptors can inhibit the release of nitric oxide. The aim of the present study was to examine the effect of alpha1- and alpha2-adrenoceptor activation on nitric oxide-mediated vasodilation. In a first set of experiments, the endothelium-dependent vasodilators acetylcholine (ACh), 5-hydroxytryptamine (5HT), and bradykinin (BK), and the nitric oxide donor sodium nitroprusside (SNP) were administered in a random order in the brachial artery together with saline, or the nonselective alpha-adrenoceptor agonists norepinephrine or clonidine, or the nitric oxide synthase inhibitor NG-monomethyl-L-arginine (L-NMMA). The infusions of saline, norepinephrine, clonidine, and L-NMMA started 10 minutes before the infusions of ACh, BK, 5HT, and SNP. In a second set of experiments, cumulative doses of ACh, BK, and 5HT were infused, in a random order, intra-arterially together with saline or the selective alpha1-adrenoceptor agonist methoxamine. The infusions of saline and methoxamine started 5 minutes before the infusions of ACh, BK, and 5HT. Forearm blood flow was measured using computerized venous occlusion plethysmography. ACh, 5HT, BK, and SNP induced a significant increase in forearm blood flow (p < 0.05 for all). These vasodilator responses were significantly attenuated by norepinephrine, clonidine, and L-NMMA (p <0.05 for all), except for SNP. In the second set of experiments, all three endothelium-dependent vasodilators induced a dose-dependent vasodilation, which was significantly inhibited by methoxamine (p <0.05).
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These results show that endothelium-dependent nitric oxide-mediated vasodilation is inhibited by activation of peripheral alpha1-adrenoceptors. Final Decision: yes