1. Carbachol, phenylephrine and substance P were each capable of producing a transient release of K (86 Rb) from rat parotid slices in the absence of extracellular Ca. 2. Each of the agonists was also capable of producing "cross-receptor inactivation"; that is, if a transient response was elicited by any one of the agonists then no transient response could be obtained by either of the other two. 3. 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. 4. It is concluded that the K release response in the parotid gland is mediated by receptor-controlled Ca influx sites. These influx sites also bind Ca at a location inaccessible to EGTA and release the bound Ca upon receptor activation. 5. It is also conlcuded that all three receptors (muscarinic, alpha-adrenergic, and peptide) appear to regulate the same Ca influx sites.