Molecular Pharmacology, Vol 14, 1046-1053, Copyright © 1978 by the American Society for Pharmacology and Experimental Therapeutics

Receptor Control of Calcium Influx in Parotid Acinar Cells

¹ Department of Pharmacology, Wayne State University School of Medicine, Detroit, Michigan, 48201

The effects of various agonists and antagonists on Ca⁺⁺ influx in dispersed rat parotid acinar cells were investigated. The cell preparation was first characterized. The cells maintained normal ultrastructure and physiological content of Na⁺ and K⁺, and secreted amylase or K in response to appropriate secretagogues. Uptake of ⁴⁵Ca was stimulated by carbachol, epinephrine, substance P and isoproterenol. Isoproterenol, but not carbachol, stimulated uptake of [¹⁴C]sucrose and caused a decrease in protein content per aliquot of cells. These latter observations suggest that the increased Ca⁺⁺ uptake due to beta adrenergic stimulation may, at least in part, result from pinocytosis. The stimulated ⁴⁵Ca uptake due to either carbachol or substance P was blocked by 3.0 mM CoCl₂. Procaine (1.0 mM), however, blocked the response to carbachol but not substance P. These results support an hypothesis suggesting that Co⁺⁺ blocks inward transport of Ca⁺⁺ while procaine interferes with the transduction mechanism linking the muscarinic receptor to the Ca⁺⁺ channel.