Nitric oxide contributes to the regulation of vasomotor tone but does not modulate O2-consumption in exercising swine

Abstract

Objective: The role of nitric oxide (NO) in the regulation of vasomotor tone and tissue O2-consumption is incompletely understood. We therefore determined the contribution of endogenous NO to regulation of systemic, pulmonary and coronary vasomotor tone and myocardial (MVo2) and whole body (BVo2) O2-consumption in exercising swine. Methods and results: Exercise (1-5 km/h) up to 85% of maximum heart rate in 11 swine produced a 4-fold increase in BVo2, which was accommodated for by 2-fold increases in both cardiac output (CO) and body O2-extraction. The NO synthase inhibitor N(ω)- nitro-L-arginine (NLA, 20 mg/kg, i.v.) increased mean aortic pressure by 30 mmHg both at rest and during exercise, due to a decrease in systemic vascular conductance from 37 ± 2 to 22 ± 1 ml/min mmHg-1 at rest and from 88 ± 3 to 60 ± 3 ml/min mmHg-1 at 5 km/h (all P ≤ 0.05 versus control). NLA produced vasoconstriction at rest and at 5 km/h in virtually all regional beds but did not affect the exercise-induced redistribution of CO. NLA increased mean pulmonary artery pressure from 15 ± 1 to 21 ± 1 mmHg at rest and from 30 ± 2 to 40 ± 2 mmHg at 5 km/h, due to a decrease in pulmonary vascular conductance (all P ≤ 0.05). BVo2 remained unchanged and consequently the decrease in CO resulted in a compensatory increase in O2- extraction. NLA in a dose of 40 mg/kg produced similar responses. NLA had no significant effect on myocardial O2-demand or MVo2 either at rest or during exercise, but decreased coronary vascular conductance which resulted in a decrease in coronary venous Po2 from 24.5 ± 1.1 to 21.9 ± 0.8 mmHg at rest and from 23.5 ± 0.5 to 21.0 ± 0.6 mmHg at 5 km/h (all P ≤ 0.05). Conclusions: Endogenous NO dilates the systemic, pulmonary and coronary vascular bed, but does not modify MVo2 or BVo2 in swine at rest and during exercise. (C) 2000 Elsevier Science B.V.