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Research Article Free access | 10.1172/JCI117020

Exercise-induced pulmonary vasoconstriction during combined blockade of nitric oxide synthase and beta adrenergic receptors.

D W Kane, T Tesauro, T Koizumi, R Gupta, and J H Newman

Center for Lung Research, Vanderbilt University School of Medicine, Nashville, Tennessee 37232.

Find articles by Kane, D. in: JCI | PubMed | Google Scholar

Center for Lung Research, Vanderbilt University School of Medicine, Nashville, Tennessee 37232.

Find articles by Tesauro, T. in: JCI | PubMed | Google Scholar

Center for Lung Research, Vanderbilt University School of Medicine, Nashville, Tennessee 37232.

Find articles by Koizumi, T. in: JCI | PubMed | Google Scholar

Center for Lung Research, Vanderbilt University School of Medicine, Nashville, Tennessee 37232.

Find articles by Gupta, R. in: JCI | PubMed | Google Scholar

Center for Lung Research, Vanderbilt University School of Medicine, Nashville, Tennessee 37232.

Find articles by Newman, J. in: JCI | PubMed | Google Scholar

Published February 1, 1994 - More info

Published in Volume 93, Issue 2 on February 1, 1994
J Clin Invest. 1994;93(2):677–683. https://doi.org/10.1172/JCI117020.
© 1994 The American Society for Clinical Investigation
Published February 1, 1994 - Version history
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Abstract

We studied the effects of inhibition of nitric oxide (NO) (endothelium-derived relaxation factor) synthase in combination with alpha and beta adrenergic receptor blockade on pulmonary vascular tone during exercise. In paired studies, we exercised sheep on a treadmill at a speed of 4 mph, and measured blood flow and pressures across the pulmonary circulation with and without inhibition of NO synthase (N omega-nitro-L-arginine 20 mg/kg intravenous [i.v.]), alpha receptor blockade (phentolamine 5 mg i.v.), beta receptor blockade (propranolol 1 mg i.v.), and combined alpha and beta receptor blockade. Activation of both types of adrenergic receptors occurs with exercise, and because increased release in NO is hypothesized to occur during exercise, these studies were designed to determine the magnitude of effect and interactions of these competing dilator and constrictor influences. We found that inhibition of NO synthase raised pulmonary vascular resistance (PVR) at rest and that, although a reduction in PVR occurred with exercise from this new baseline, vasoconstriction persisted. Combined beta blockade and NO synthase inhibition unmasked unopposed alpha vasoconstriction; PVR rose at rest and continued to rise with exercise; and mean pulmonary arterial pressures approached very high levels, 43.8 +/- 4.4 cmH2O. Using a distal wedged pulmonary artery catheter technique, most of the vasoconstriction was found to be in vessels upstream from small pulmonary veins. During exercise in sheep there appears to be a high degree of alpha and beta adrenergic-mediated tone in the pulmonary circulation. Endogenous production of NO actively dilates pulmonary vessels at rest and opposes potent alpha-mediated pulmonary vasoconstriction during exercise.

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