Abstract
1 Experiments were performed on cats anaesthetized with pentobarbitone in which carotid chemoreceptor activity was recorded from the peripheral end of a sectioned carotid sinus nerve. 2 Intracarotid injections of adenosine 5′-triphosphate (ATP) (1–100 μg i.e.) caused a dose-related increase in chemosensory discharge which was delayed in onset. 3 The adenosine uptake inhibitor dipyridamole potentiated the chemoexcitatory effects of injected adenosine and ATP. 4 The stable ATP analogue α-β-methylene ATP (10–100 μg i.c.) depressed chemoreceptor discharge, which suggests the presence of a P2-purinoceptor in the carotid body, and provides evidence that the chemoexcitatory effect of ATP results from its hydrolysis to adenosine 5′-phosphate (AMP)/adenosine. 5 Adenine, inosine, guanosine, cytidine and uridine had no appreciable effect on chemoreceptor discharge. 6 The adenosine R-site agonists 2′-chloroadenosine and N6-methyladenosine had chemoexcitatory effects which were similar to those of adenosine, whereas the P-site agonist 2′-deoxyadenosine had no appreciable effect on discharge. 7 We conclude that the adenosine receptor in the cat carotid body has some of the characteristics of an R-site receptor according to the classification of Londos & Wolff (1977).