Are there purinergic receptors on parotid acinar cells?

Abstract

ATP and other purine nucleotides and nucleosides have potent regulatory (neurotransmitter-like) actions which have been attributed to interaction with a specific plasma membrane receptor¹. To date the receptor mechanisms underlying purinergic activation have been poorly characterized. One problem has been the variability of the evoked effects in different tissues. Burnstock^2,3 proposed that much of the variability could be explained if the effects were mediated by two separate receptors, termed P₁ and P₂, with different specificities for agonists and antagonists. Receptor mechanisms have been extensively investigated in the parotid gland⁴. I now report that in that gland, ATP evokes a marked increase in membrane conductance, radioactive Rb efflux and amylase secretion. The effects of ATP are similar to those evoked by acetylcholine (ACh) and α-adrenergic agonists but are still present when cholinergic and adrenergic blocking agents are used. The latency and reversal potential of the ATP-evoked effects are comparable with those of the autonomic agonists. The ATP receptor on parotid acinar cells is of the P₂ type^2,3, since the order of potency of the nucleotide series was ATP>ADP≫AMP, adenosine had no effect, and the response could be blocked by quinidine but not by theophylline.