Alpha 1-adrenergic and muscarinic-cholinergic stimulated inositol trisphosphate production may proceed through different post-receptor signal transduction pathways in parotid acini.

Maximal stimulation of inositol 1,4,5 trisphosphate (IP3) production by epinephrine and carbachol in rat parotid cell aggregates is additive when the two agents are employed simultaneously. The additive response proceeds through both the alpha 1-adrenergic and muscarinic-cholinergic signal transduction pathways. It is critical that IP3 be measured by a radioreceptor assay, since when cells are labeled with 3H-inositol and IP3 determined by ion exchange chromatography, additivity is not detectable. Reasons for the discrepancy between methods are discussed. These results, coupled with the differential sensitivity of the alpha 1-adrenergic and muscarinic cholinergic pathways to neomycin and aging, suggest that they may be dissociated at the post-receptor level.