Key result
ATP in concentrations between 0.05 and 2 mM increased the maximum response of the dose-response curve of ACh currents without an appreciable effect on the affinity of ACh for its receptor.
ATP increases the sensitivity of the nicotinic ACh-receptor in bullfrog sympathetic ganglion cells, likely by acting on an allosteric site.
No direct clinical implications from amphibian data; leaves open allosteric ATP effects on nicotinic receptors for mammalian studies.
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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Akasu et al. (1985) studied this question. Adenosine triphosphate (ATP) was evaluated on Amplitudes of potentials and currents induced by ACh and carbachol. ATP in concentrations between 0.05 and 2 mM increased the maximum response of the dose-response curve of ACh currents without an appreciable effect on the affinity of ACh for its receptor.
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