Further cholinergic aspects of carotid body chemotransduction of hypoxia in cats

Robert S. Fitzgerald 1 , 2 , 3 , Machiko Shirahata 1 , 4 , and Tohru Ide 1 Departments of 1 Environmental Health Sciences, 2 Physiology, 3 Medicine, and 4 Anesthesiology/Critical Care Medicine, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21205 Received 21 August 1995; accepted in final form 27 November 1996. Fitzgerald, Robert S., Machiko Shirahata, and Tohru Ide. Further cholinergic aspects of carotid body chemotransduction of hypoxia in cats. J. Appl. Physiol. 82(3): 819-827, 1997. From the 1930s into the 1970s, the role of acetylcholine (ACh) in the carotid body's chemotransduction of hypoxia was debated. Since the late 1970s, the issue has been pursued only intermittently or not at all. The purpose of this study was to test again with a new preparation the hypothesis that ACh is an excitatory neurotransmitter in the cat carotid body's chemotransduction of hypoxia. We tested the effect of the specific nicotinic blocker mecamylamine and the muscarinic blocker of all five muscarinic receptors, atropine. We further tested the effects of M 1 and M 2 muscarinic-receptor blockers. The carotid body region was selectively perfused with hypoxic Krebs-Ringer bicarbonate (KRB) solutions that were blocker free or contained varying doses of the blockers. Both mecamylamine and atropine reduced the response to hypoxic KRB in a dose-related manner. The M 2 muscarinic-receptor blockers gallamine and AFDX 116 increased the response to hypoxic KRB, whereas the M 1 muscarinic-receptor blocker pirenzepine reduced the response to hypoxic KRB. These data are consistent with an excitatory role for ACh in the carotid body chemotransduction of hypoxia in the cat. acetylcholine; mecamylamine; atropine; gallamine; pirenzepine; AFDX 116 0161-7567/97 $5.00 Copyright © 1997 the American Physiological Society