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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
M1 and
M2 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
M2 muscarinic-receptor blockers
gallamine and AFDX 116 increased the response to hypoxic KRB, whereas
the M1 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
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