Nitric oxide contributes to the rise in forearm blood flow during mental stress in humans.

Abstract

1. Our aim was to determine whether the vasodilating substance nitric oxide (NO) contributes to the rise in forearm blood flow observed during mental stress in humans. We also determined whether the NO might be released as a result of cholinergic stimulation of the vascular endothelium. 2. Blood flow was measured in both forearms using plethysmography during several 3‐5 min bouts of a colour word test. In one forearm the nitric oxide synthase blocker NG‐monomethyl‐L‐arginine (L‐NMMA) and other drugs were infused via a brachial artery catheter. The contralateral forearm served as a control. 3. When L‐NMMA was given prior to mental stress it blunted the rise in blood flow in the treated forearm almost completely. The normal blood flow response returned during a second bout of stress conducted after a wash‐out period. During a third 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 the treated forearm. Subsequent administration of both atropine and L‐NMMA caused a somewhat greater reduction in the blood flow responses than those observed with atropine alone. 5. These data demonstrate that NO plays a role in forearm vasodilatation during mental stress in humans. It is likely that most of the NO is released by cholinergic stimulation of the vascular endothelium.

Racial Differences in Nitric Oxide–Mediated Vasodilator Response to Mental Stress in the Forearm Circulation

“…13,14 Importantly, a reduction in NO activity has been widely demonstrated in hypertensive patients [15][16][17][18][19][20] and, more recently, even in normotensive offspring of hypertensive parents 21 ; these findings support the concept that decreased action of NO might play a pathophysiological role in the development of hypertension. It is therefore reasonable to hypothesize that a decreased vascular activity of NO also could be involved in the abnormal hemodynamic reactivity pattern to stress and the increased susceptibility to developing high blood pressure over repeated exposures to stressful situations that are observed in African Americans.…”

Cardiovascular and renal responses to mental challenge in highly and moderately active males with a family history of hypertension

“…The locally released acetylcholine is then thought to act on muscarinic receptors and cause nitric oxide release producing vasodilatation. 26 Exercise-induced reactivity lowering mechanism Differences in sympathetic withdrawal, ␤-adrenergic receptor activation, and/or local vasodilatation mechanisms may explain the difference in FBF reactivity to mental challenge between the moderately and highly active offspring hypertensives. However, it is interesting to note that the forearm vasodilatation response was only significantly different between the groups during the initial first 2 min of the mental challenge.…”

Bimodal distribution of vasodilator responsiveness to adenosine due to difference in nitric oxide contribution: implications for exercise hyperemia

“…The brachial artery of the nondominant forearm was catheterized under aseptic conditions after local anesthesia (1% lidocaine). A standard 5-cm, 20-gauge Teflon catheter was inserted and connected to a three-port connector system for simultaneous measurements of arterial pressure and local administration of study drugs (5).…”