NITRIC-OXIDE CONTRIBUTES TO THE RISE IN FOREARM BLOOD-FLOW DURING MENTAL STRESS IN HUMANS

1. Our aim was to determine whether the vasodilating substance nitric oxide (NO) contributes to the rise in forearm blood flow observed duri ng mental stress in humans. We also determined whether the NO might be released as a result of cholinergic stimulation of the vascular endot helium. 2. Blood flow was measured in both forearms using plethysmogra phy during several 3-5 min bouts of a colour word test. In one forearm the nitric oxide synthase blocker N-G-monomethyl-L-arginine (L-NMMA) and other drugs were infused via a brachial artery catheter. The contr alateral forearm served as a control. 3. When L-NMMA was given prior t o mental stress it blunted the rise in blood flow in the treated forea rm almost completely. The normal blood flow response returned during a second bout of stress conducted after a wash-out period. During a thi rd bout of mental stress, administration of more L-NMMA again blunted the blood flow responses to mental stress. 4. When atropine was given prior to mental stress, the increases in blood flow were reduced in th e treated forearm. Subsequent administration of both atropine and L-NM MA caused a somewhat greater reduction in the blood flow responses tha n those observed with atropine alone. 5. These data demonstrate that N O plays a role in forearm vasodilatation during mental stress in human s. It is likely that most of the NO is released by cholinergic stimula tion of the vascular endothelium.