The parotid gland of the aged rat provides an example of an altered α 1-adrenergic physiologic response (K + efflux) resulting from a postreceptor perturbation in signal transduction mechanisms. This is alteration in gland function can be completely circumvented by eliciting K + efflux via the Ca 2+-ionophore, A23187, at several Ca 2+ concentrations. Since Ca 2+ is purported to mediate other secretory events in the rat parotid, we have probed neurotransmitter regulated Ca 2+ mobilization and secretory mechanisms in this tissue by employing an aging paradigm. The responses studied were α-adrenergic- and muscarinic-cholinergic-mediated K + efflux, 45Ca 2+ release, and amylase secretion. No differences were detected between young (3 months) and old (24 months) cell preparations for any muscarinic-cholinergic agonist-induced response studied. Following α-adrenergic stimulation, K + efflux and 45Ca 2+ release from old cell preparations were reduced markedly, while no changes were found for the amylase secretion response. These results suggest that 1) α-adrenergic and cholinergic signal transduction mechanisms for K + efflux and 45Ca 2+ release are dissociated in cells of the rat parotid gland, and 2) following α 1-adrenergic stimulation, signal transduction likely proceeds by at least two pathways, one which is apparently involved in protein excytosis (intact in cells from old rats) and the other which is apparently involved in K + efflux and 45Ca 2+ release (perturbed in old cells).
|Number of pages||4|
|Journal||Journal of Biological Chemistry|
|State||Published - 16 Jun 1983|