Nitric oxide contributes to the regulation of vasomotor tone but does not modulate O-2-consumption in exercising swine

Citation
Dj. Duncker et al., Nitric oxide contributes to the regulation of vasomotor tone but does not modulate O-2-consumption in exercising swine, CARDIO RES, 47(4), 2000, pp. 738-748
Citations number
40
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
CARDIOVASCULAR RESEARCH
ISSN journal
00086363 → ACNP
Volume
47
Issue
4
Year of publication
2000
Pages
738 - 748
Database
ISI
SICI code
0008-6363(200009)47:4<738:NOCTTR>2.0.ZU;2-Q
Abstract
Objective: The role of nitric oxide (NO) in the regulation of vasomotor ton e and tissue O-2-consumption is incompletely understood. We therefore deter mined the contribution of endogenous NO to regulation of systemic, pulmonar y 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 increas e 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-nit ro-L-arginine (NLA, 20 mg/kg, i.v.) increased mean aortic pressure by 30 mm Hg 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 mmH g at rest and from 30+/-2 to 40+/-3 mmHg at 5 km/h, due to a decrease in pu lmonary vascular conductance (all P less than or equal to 0.05). BVo(2) rem ained unchanged and consequently the decrease in CO resulted in a compensat ory 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 conduct ance which resulted in a decrease in coronary venous Po-2 from 24.5+/-1.1 t o 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) o r BVo(2) in swine at rest and during exercise. (C) 2000 Elsevier Science B. V. All rights reserved.