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Science 18 September 1981:
Vol. 213. no. 4514, pp. 1376 - 1379
DOI: 10.1126/science.7268440
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Articles

Science, Vol 213, Issue 4514, 1376-1379
Copyright © 1981 by American Association for the Advancement of Science

articles

Acetylcholine and bradykinin relax intrapulmonary arteries by acting on endothelial cells: role in lung vascular diseases

N Chand and BM Altura

Acetylcholine and bradykinin produced potent relaxation of isolated canine intrapulmonary arteries contracted by serotonin, norepinephrine, or phenylephrine-provided the endothelium was left intact. Selective mechanical destruction of the endothelium transformed the activity of these substances from vasodilatation to vasoconstriction. Acetylcholine-induced relaxations, in the presence of intact endothelium, could be selectively inhibited competitively by atropine, but could not be inhibited by cyclooxygenase inhibitors, a lipoxygenase inhibitor, adrenergic blocking drugs, or histaminergic antagonists. RElaxations produced by prostacyclin, prostaglandin E1, isoproterenol, papaverine, or histamine H2-receptor agonists were not modified, or attenuated, by selective destruction of pulmonary endothelial cells. These observations might provide insight into the etiology of the increased pulmonary resistance observed in pulmonary hypertension and shock lung.


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