Evidence that catecholamines increase acetylcholine release from neuromuscular junction through stimulation of alpha-1 adrenoceptors.
1. The effects of alpha-1 adrenoceptor agonists on 3H-acetylcholine release from mouse phrenic nerve-hemidiaphragm preparation were studied. 2. In preparation which had been incubated with 3H-choline, electrical stimulation (50 Hz, 0.8 s trains every 10 s) released 3H-acetylcholine. Neurochemical evidence was obtained that noradrenaline, adrenaline and phenylephrine facilitated the stimulation evoked release of 3H-acetylcholine. This effect was much more marked when the prejunctional nicotinic receptors mediating positive feedback modulation were blocked by (+)-tubocurarine. In the presence of this drug, when the release of 3H-acetylcholine was reduced, alpha-1 adrenoceptor agonists enhanced the release in a prazosin-sensitive manner. 3. The rank order of potency of alpha-1 adrenoceptor agonists was adrenaline greater than noradrenaline greater than phenylephrine. By contrast, methoxamine had no effect on the release of 3H-acetylcholine. It is suggested, therefore, that circulating catecholamines may be able to affect neuromuscular transmission through stimulation of presynaptic alpha-1 adrenoceptors.
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Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest.
D000109:Acetylcholine / Q000378:metabolism*; D000818:Animals; D002395:Catecholamines / Q000494:pharmacology*; D066298:In Vitro Techniques; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D009469:Neuromuscular Junction / Q000378:metabolism / Q000502:physiology*; D010791:Phrenic Nerve / Q000378:metabolism; D011942:Receptors, Adrenergic, alpha / Q000187:drug effects*; D009435:Synaptic Transmission; D014316:Tritium
D002395:Catecholamines; D011942:Receptors, Adrenergic, alpha; D014316:Tritium; D000109:Acetylcholine