Hemodynamic and sympathoadrenal responses to mental stress during nitric oxide synthesis inhibition

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Abstract
Cardiovascular and sympathoadrenal responses to a reproducible mental stress test were investigated in eight healthy young men before and during intravenous infusion of the nitric oxide (NO) synthesis inhibitor N-monomethyl-l-arginine (l-NMMA). Before l-NMMA, stress responses included significant increases in heart rate, mean arterial pressure, and cardiac output (CO) and decreases in systemic and forearm vascular resistance. Arterial plasma norepinephrine (NE) increased. At rest after 30 min of infusion of l-NMMA (0.3 mg·kg−1·min−1 iv), mean arterial pressure increased from 98 ± 4 to 108 ± 3 mmHg ( P < 0.001) because of an increase in systemic vascular resistance from 12.9 ± 0.5 to 18.5 ± 0.9 units ( P < 0.001). CO decreased from 7.7 ± 0.4 to 5.9 ± 0.3 l/min ( P < 0.01). Arterial plasma NE decreased from 2.08 ± 0.16 to 1.47 ± 0.14 nmol/l. Repeated mental stress during continued infusion of l-NMMA (0.15 mg·kg−1·min−1) induced qualitatively similar cardiovascular responses, but there was a marked attenuation of the increase in mean arterial blood pressure, resulting in similar “steady-state” blood pressures during mental stress without and with NO blockade. Increases in heart rate and CO were attenuated, but stress-induced decreases in systemic and forearm vascular resistance were essentially unchanged. Arterial plasma NE increased less than during the first stress test. Thus the increased arterial tone at rest during l-NMMA infusion is compensated for by attenuated increases in blood pressure during mental stress, mainly through a markedly attenuated CO response and suppressed sympathetic nerve activity.