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

Objective: The role of nitric oxide (NO) in the regulation of vasomotor tone and tissue O-2-consumption is incompletely understood. We therefore determined the contribution of endogenous NO to regulation of systemic, pulmonary and coronary vasomotor tone and myocardial (MVo(2)) and whole body (BVo(2)) O-2-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 BVo(2), which was accommodated for by 2-fold increases in both cardiac output (CO) and body O-2-extraction. The NO synthase inhibitor N-omega-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 less than or equal to 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+/-3 mmHg at 5 km/h, due to a decrease in pulmonary vascular conductance (all P less than or equal to 0.05). BVo(2) remained unchanged and consequently the decrease in CO resulted in a compensatory increase in O-2-extraction. NLA in a dose of 40 mg/kg produced similar responses. NLA had no significant effect on myocardial O-2-demand or MVo(2) either at rest or during exercise, but decreased coronary vascular conductance which resulted in a decrease in coronary venous Po-2 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 less than or equal to 0.05). Conclusions: Endogenous NO dilates the systemic, pulmonary and coronary vascular bed, but does not modify MVo(2) or BVo(2) in swine at rest and during exercise. (C) 2000 Elsevier Science B.V. All rights reserved.