Muscarinic, alpha‐adrenergic and peptide receptors regulate the same calcium influx sites in the parotid gland.

Abstract

Carbachol, phenylephrine and substance P were each capable of producing a transient release of K (86Rb) from rat parotid slices in the absence of extracellular Ca. Each of the agonists was also capable of producing cross-receptor inactivation; i.e., if a transient response was elicited by any 1 of the agonists then no transient response could be obtained by either of the other 2. Removal of carbachol from muscarinic receptors with atropine did not reverse the cross-receptor inactivation of the substance P response unless Ca was added with substance P or unless Ca was present when atropine was added. The K release response in the parotid gland appears to be mediated by receptor-controlled Ca influx sites. These influx sites also bind Ca at a location inaccessible to EGTA [ethyleneglycol-bis(aminoethylether)-N,N''-tetraacetic acid] and release the bound Ca upon receptor activation. All 3 receptors (muscarinic, .alpha.-adrenergic, and peptide) appear to regulate the same Ca influx sites. The parotid gland of the rat is an excellent tool for the study of the early events following receptor activation because of the existence of at least 3 distinct receptor systems activating the same physiological process.