ANALYSIS OF THE VASOPRESSOR AND OTHER "NICOTINIC" ACTIONS OF ACETYLCHOLINE

Abstract

The anti-cholinesterases, physostigmine and prostigmin, potentiated the pressor effect of acetylcholine but not that of muscarine and doryl. Small doses of acetyleholine in the presence of physostigmine or prostigmin produced acceleration of the heart, relaxation of the gut, stimulation of the ocular sympathetic, inco-ordinated somatic motor efforts and stimulation of respiration in atropinized animals. The pressor effects produced by acetylcholine were preserved following removal of the carotid sinuses, the C. N. S., the adrenal glands, the liver, and/or clamping of the abdominal aorta at the level of the diaphragm. Upon the removal of the thoracic sympathetic and the superior cervical ganglia, acetylcholine did not produce pressor effects or other nicotinic actions following clamping of the abdominal aorta. Thus the site of the pressor effect was localized in the sympathetic ganglia. The substance or substances liberated by acetylcholine stimulation of the sympathetic ganglia might be transferred from 1 animal to another, producing pressor effects in the recipient. Cocaine did not initiate pressor responses from small ineffective doses of acetylcholine in atropinized animals, but it enhanced these effects from effective doses of acetylcholine.