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Acetylcholine and Bradykinin Relax Intrapulmonary Arteries by Acting on Endothelial Cells: Role in Lung Vascular Diseases

Naresh Chand and Burton M. Altura
Science
New Series, Vol. 213, No. 4514 (Sep. 18, 1981), pp. 1376-1379
Stable URL: http://www.jstor.org/stable/1686474
Page Count: 4
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Acetylcholine and Bradykinin Relax Intrapulmonary Arteries by Acting on Endothelial Cells: Role in Lung Vascular Diseases
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Abstract

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 E$_{1}$, isoproterenol, papaverine, or histamine H$_{2}$-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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