Evidence that endogenous catecholamines can regulate acetylcholine release in a sympathetic ganglion.
The objective of this study was to test whether activation of alpha-adrenoceptors by endogenously released catecholamines alters the release of acetylcholine (ACh) from the cat superior cervical ganglion. The alpha-adrenoceptor agonists noradrenaline and clonidine depressed evoked ACh release; this effect was concentration-dependent; it was apparent during preganglionic stimulation at 20 Hz, but not so at lower frequencies of stimulation. The inhibitory effect of noradrenaline on evoked ACh release was reversed by yohimbine, by phentolamine and, to a lesser extent, by prazosin. Thus, exogenous amines can depress evoked ACh release by an action on presynaptic alpha-adrenoceptors. To determine if activation of these receptors by endogenous amines inhibits ACh release, we tested whether the alpha-adrenoreceptor antagonists enhance ACh release. Yohimbine and phentolamine increased evoked ACh release during preganglionic stimulation at 20 Hz, but not during stimulation at 5 Hz, suggesting that endogenous, like exogenous, amine can depress evoked ACh release from preganglionic nerve terminals.
D000109:Acetylcholine / Q000378:metabolism*; D000818:Animals; D002415:Cats; D003000:Clonidine / Q000494:pharmacology; D004558:Electric Stimulation; D005260:Female; D005728:Ganglia, Sympathetic / Q000378:metabolism*; D008297:Male; D009638:Norepinephrine / Q000037:antagonists & inhibitors / Q000494:pharmacology / Q000502:physiology*; D010646:Phentolamine / Q000494:pharmacology; D011224:Prazosin / Q000494:pharmacology; D015016:Yohimbine / Q000494:pharmacology
D015016:Yohimbine; D003000:Clonidine; D000109:Acetylcholine; D009638:Norepinephrine; D011224:Prazosin; D010646:Phentolamine