Abstract
The effects of adenosine triphosphate (ATP) and related compounds on the sensitivity of the nicotinic acetylcholine (ACh)-receptor of bullfrog sympathetic ganglion cells were analysed electro-physiologically. ATP in concentrations between 0.05 and 2 mM increased the amplitudes of the potentials and currents induced by ACh, and carbachol-induced currents. Compared with ATP, ADP was less potent in producing augmentation of the carbachol-induced current by one order of magnitude. AMP, cyclic AMP and adenosine had no appreciable effect. Analysis of this ATP effect, based on Michaelis-Menten type kinetics, revealed that ATP increased the maximum response (Vmax) of the dose-response curve of ACh currents without an appreciable effect on the affinity (Km) of ACh for its receptor. It is suggested that ATP increased the receptor sensitivity by acting on an allosteric site of the nicotinic ACh receptor-ionic channel complex which, thus, may be linked to an ATP receptor, probably of the P2-receptor type (Burnstock, 1981).
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