Acetylcholine — Prostanoid Interaction in the Pulmonary Circulation

Abstract

Parasympathetic innervation of pulmonary arteries and/or veins has been identified histologically in many species and is achieved via the tenth cranial nerve (vagus; 5, 6). The pulmon- ary hemodynamic alterations resulting from vagal stimulation or administration of muscarinic agonists, however, remain controversial. Over the last fifty years, sporadic investigations have proposed that acetylcholine (ACh) causes vasoconstriction in the pulmonary circulation of the dog, monkey, rabbit, rat, guinea pig, cat, frog and sheep; however others have observed vasodilation in the pulmonary circulation of dog, cat and pig (for review, see ref. 1). Some of the factors that could be responsible for the apparent discrepancy in these findings include adrenergic discharge or concomitant bronchoconstriction contributing to pulmonary vasoconstriction, and cholinergic — induced bradycardia, systemic hypotension and decreased cardiac output causing secondary pulmonary vasodilation.