title: Nitric oxide contributes to the regulation of vasomotor tone but does not modulate O(2)-consumption in exercising swine.
abstract: 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 (MV(O(2))) and whole body (BV(O(2))) O(2)-consumption in exercising swine.
  
  
  RESULTS
  Exercise (1-5 km/h) up to 85% of maximum heart rate in 11 swine produced a 4-fold increase in BV(O(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< or =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< or =0.05). BV(O(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 MV(O(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< or =0. 05).
  
  
  CONCLUSIONS
  Endogenous NO dilates the systemic, pulmonary and coronary vascular bed, but does not modify MV(O(2)) or BV(O(2)) in swine at rest and during exercise.
authors.affiliation: Experimental Cardiology, Thoraxcenter, Erasmus University Rotterdam, P.O. Box 1738, 3000 DR Rotterdam, The Netherlands. duncker@tch.fgg.eur.nl
authors.forename: D J
authors.initials: DJ
authors.lastname: Duncker
authors.forename: R
authors.initials: R
authors.lastname: Stubenitsky
authors.forename: P A
authors.initials: PA
authors.lastname: Tonino
authors.forename: P D
authors.initials: PD
authors.lastname: Verdouw
mesh_terms: D000818:Animals; D003326:Coronary Circulation / Q000187:drug effects; D004285:Dogs; D004791:Enzyme Inhibitors / Q000494:pharmacology; D015444:Exercise / Q000502:physiology*; D005260:Female; D006801:Humans; D008297:Male; D018482:Muscle, Skeletal / Q000098:blood supply; D009206:Myocardium / Q000378:metabolism*; D009569:Nitric Oxide / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D019335:Nitroarginine / Q000494:pharmacology; D010101:Oxygen Consumption / Q000187:drug effects*; D011652:Pulmonary Circulation / Q000187:drug effects; D012039:Regional Blood Flow / Q000187:drug effects; D013045:Species Specificity; D013552:Swine; D014655:Vascular Resistance / Q000187:drug effects*; D014662:Vasoconstrictor Agents / Q000494:pharmacology
chemical_list: D004791:Enzyme Inhibitors; D014662:Vasoconstrictor Agents; D019335:Nitroarginine; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase