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Changes in pulmonary vascular tone during exercise. Effects of nitric oxide (NO) synthase inhibition, L-arginine infusion, and NO inhalation.
J Clin Invest. 1994 Dec; 94(6):2275-82.JCI

Abstract

Nitric oxide (NO) is a potent endogenous vasodilator. Its role in the normal and stressed pulmonary circulation is unclear. To better understand the importance of endogenous NO in normal physiological responses, we studied the effects of altered NO availability on the change in pulmonary vascular tone that accompanies exercise. In paired studies we measured blood flow and pressures in the pulmonary circulation at rest and during treadmill exercise at a speed of 4 mph with and without (a) N omega-nitro-L-arginine, 20 mg/kg intravenously, a selective inhibitor of NO synthase; (b) L-arginine, 200 mg/kg intravenously, substrate for NO synthase; (c) combination of the inhibitor and substrate; and (d) inhalation of NO > 30 ppm, to determine if endogenous release of NO elicits maximal vasodilation. In addition, we sought to determine the site of NO effect in the pulmonary circulation by preconstriction with either U-44619 or hypoxia (fraction of inspired O2 = 0.12) using a distal wedged pulmonary catheter technique. NO synthase inhibition raised pulmonary vascular tone equally at rest and exercise. L-Arginine reversed the effects of NO synthase inhibition but had no independent effect. NO inhalation did not reduce pulmonary vascular tone at rest or enhance the usual reduction in pulmonary vascular resistance with exercise. The effect of NO synthase inhibition was in pulmonary vessels upstream from small veins, suggesting that endogenous NO dilates primarily small arteries and veins at rest. We conclude that, in sheep, endogenous NO has a basal vasodilator function that persists during, but is not enhanced by, exercise.

Authors+Show Affiliations

Vanderbilt Center for Lung Research, Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 37232-2650.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

7527429

Citation

Koizumi, T, et al. "Changes in Pulmonary Vascular Tone During Exercise. Effects of Nitric Oxide (NO) Synthase Inhibition, L-arginine Infusion, and NO Inhalation." The Journal of Clinical Investigation, vol. 94, no. 6, 1994, pp. 2275-82.
Koizumi T, Gupta R, Banerjee M, et al. Changes in pulmonary vascular tone during exercise. Effects of nitric oxide (NO) synthase inhibition, L-arginine infusion, and NO inhalation. J Clin Invest. 1994;94(6):2275-82.
Koizumi, T., Gupta, R., Banerjee, M., & Newman, J. H. (1994). Changes in pulmonary vascular tone during exercise. Effects of nitric oxide (NO) synthase inhibition, L-arginine infusion, and NO inhalation. The Journal of Clinical Investigation, 94(6), 2275-82.
Koizumi T, et al. Changes in Pulmonary Vascular Tone During Exercise. Effects of Nitric Oxide (NO) Synthase Inhibition, L-arginine Infusion, and NO Inhalation. J Clin Invest. 1994;94(6):2275-82. PubMed PMID: 7527429.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Changes in pulmonary vascular tone during exercise. Effects of nitric oxide (NO) synthase inhibition, L-arginine infusion, and NO inhalation. AU - Koizumi,T, AU - Gupta,R, AU - Banerjee,M, AU - Newman,J H, PY - 1994/12/1/pubmed PY - 1994/12/1/medline PY - 1994/12/1/entrez SP - 2275 EP - 82 JF - The Journal of clinical investigation JO - J Clin Invest VL - 94 IS - 6 N2 - Nitric oxide (NO) is a potent endogenous vasodilator. Its role in the normal and stressed pulmonary circulation is unclear. To better understand the importance of endogenous NO in normal physiological responses, we studied the effects of altered NO availability on the change in pulmonary vascular tone that accompanies exercise. In paired studies we measured blood flow and pressures in the pulmonary circulation at rest and during treadmill exercise at a speed of 4 mph with and without (a) N omega-nitro-L-arginine, 20 mg/kg intravenously, a selective inhibitor of NO synthase; (b) L-arginine, 200 mg/kg intravenously, substrate for NO synthase; (c) combination of the inhibitor and substrate; and (d) inhalation of NO > 30 ppm, to determine if endogenous release of NO elicits maximal vasodilation. In addition, we sought to determine the site of NO effect in the pulmonary circulation by preconstriction with either U-44619 or hypoxia (fraction of inspired O2 = 0.12) using a distal wedged pulmonary catheter technique. NO synthase inhibition raised pulmonary vascular tone equally at rest and exercise. L-Arginine reversed the effects of NO synthase inhibition but had no independent effect. NO inhalation did not reduce pulmonary vascular tone at rest or enhance the usual reduction in pulmonary vascular resistance with exercise. The effect of NO synthase inhibition was in pulmonary vessels upstream from small veins, suggesting that endogenous NO dilates primarily small arteries and veins at rest. We conclude that, in sheep, endogenous NO has a basal vasodilator function that persists during, but is not enhanced by, exercise. SN - 0021-9738 UR - https://www.unboundmedicine.com/medline/citation/7527429/Changes_in_pulmonary_vascular_tone_during_exercise__Effects_of_nitric_oxide__NO__synthase_inhibition_L_arginine_infusion_and_NO_inhalation_ L2 - https://doi.org/10.1172/JCI117590 DB - PRIME DP - Unbound Medicine ER -