The pulmonary vascular responses to peripheral and central applications of acetylcholine

Acetylcholine (ACh) applied within the pulmonary artery elicited either a pressor or depressor response in the pulmonary vascular bed of rabbits, while ACh applied at the 4th ventricle induced a depressor response only. Both responses could be blocked by atropine and the pressor response could also be blocked partially by hexamethonium and phentolamine. Damage to the sympathoinhibition center in the median area of the medulla significantly reduced the centrogenic ACh-induced depressor response in both carotid and pulmonary arteries; the response could also be greatly diminished by the 5-HT blockers and naloxone applied centrally. It is thus suggested that ACh may exert a direct action on the M-receptors of the pulmonary vessels. It may also activate the N-receptors in the sympathetic ganglion which then induces a pulmonary vasoconstriction as a consequence. The centrogenic ACh-induced depressor responses involve the central M-receptors and are mediated by the medullary 5-HT and endorphin neuronal systems, resulting in suppression of the sympathetic tonus.