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1Division Clinical Physiology, Karolinska Institutet at Danderyd Hospital, Stockholm SE-182 88, and 2Department of Medicine, Clinical Pharmacology Unit, Karolinska Hospital, SE 171 76 Stockholm, Sweden
Submitted 22 December 2003 ; accepted in final form 28 June 2004
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·kg1·min1 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·kg1·min1) 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.
N-monomethyl-L-arginine; psychological stress; catecholamines
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