Caclium, Prostaglandins and the Phosphatidylinositol Effect in Exocrine Gland Cells

The hypothesis that arachidonic acid metabolism might be involved in Ca-mobilization mechanisms in exocrine gland cells was investigated. Arachidonate (10- super(4)M) failed to stimulate protein secretion from slices of pancreas, parotid or lacrimal glands and failed to stimulate super(86)Rb efflux from parotid or lacrimal glands. The stimulation of protein secretion (all three glands) or super(86)Rb efflux (parotid and lacrimal glands) by appropriate secretagogues was unaffected by 10 super(-5)M indomethacin. Eicosatetraynoic acid (2 x 10 super(-5)M) inhibited super(86)Rb efflux due to carbachol but not that due to physalaemin or ionomycin. Nordihydroguaiaretic acid inhibited lacrimal and parotid gland responses only at high (10 super(-4)M) concentration. Collectively, these results argue against an obligatory role for arachidonate metabolites in Ca-mediated responses of these exocrine glands.