ACETYLCHOLINE AND CAROTID-BODY EXCITATION DURING HYPOXIA IN THE CAT

Citation
Rs. Fitzgerald et M. Shirahata, ACETYLCHOLINE AND CAROTID-BODY EXCITATION DURING HYPOXIA IN THE CAT, Journal of applied physiology, 76(4), 1994, pp. 1566-1574
Citations number
44
Categorie Soggetti
Physiology
ISSN journal
87507587
Volume
76
Issue
4
Year of publication
1994
Pages
1566 - 1574
Database
ISI
SICI code
8750-7587(1994)76:4<1566:AACEDH>2.0.ZU;2-T
Abstract
The purpose of this study was to test the hypothesis that acetylcholin e (ACh) is an excitatory neurotransmitter during the hypoxic stimulati on of the carotid body. Cats were anesthetized, paralyzed, and artific ially ventilated. The common carotid artery was fitted with a loop con taining a stopcock for selectively perfusing the carotid body. Neural activity was recorded from the whole carotid sinus nerve. After the ca ts had been ventilated on 10% O-2 for 3 min with the carotid body bein g normally perfused with its own hypoxic arterial blood, the stopcock was turned, and either equally hypoxic Krebs-Ringer bicarbonate soluti on (KRB) containing alpha-bungarotoxin, mecamylamine, and atropine or hypoxic blocker-free KRB perfused the carotid body for 2 min. The stop cock was returned to its original position, allowing blocker-free hypo xic blood to perfuse the carotid body once again. With this protocol w e found 1) the cholinergic blockers reduced the carotid body response to hypoxic KRB in a dose-dependent manner; 2) carotid baroreceptor act ivity was not reduced by the blockers, suggesting that the action of t he blockers was not nonspecific (whereas lidocaine rapidly reduced bot h chemoreceptor and baroreceptor activity); 3) inclusion of the blocke rs in perfused hypoxic blood also reduced neural output from the carot id body; and 4) the blockers reduced the carotid body's neural respons e to hypoxic KRB containing substance P (20 mu g/100 ml), suggesting t hat substance P may be linked to ACh in the carotid body. We conclude that these data provide good evidence supportive of an excitatory role for ACh in carotid body hypoxic excitation.