CONTROL OF INTRACELLULAR CA-2+ BY ADRENERGIC AND MUSCARINIC AGONISTS IN MOUSE MANDIBULAR DUCTS AND ENDPIECES

The changes in free Ca2+ ([Ca2+]i) in the cells of the secretory endpieces and intralobular ducts of mouse mandibular glands exposed to adrenergic or cholinergic agonists were measured using fluorescence imaging techniques. [Ca2+]i in both cell types increased in a dose-dependent manner during both adrenergic and cholinergic stimulation. The duct cells responded to noradrenaline and to acetylcholine over the same concentration range (30 nmol/l to 3 mumol/l) although the maximum increase in [Ca2+]i above resting levels evoked by noradrenaline (ca. 137 nmol/l) was about twice that evoked by acetylcholine. The response to acetylcholine was blocked by atropine (0.1 mumol/l) and the response to noradrenaline was blocked by the alpha1-adrenergic antagonist, prazosin (0.1 mumol/l), but not by the alpha2-adrenergic antagonist, yohimbine. The alpha-adrenergic agonist, phenylephrine, mimicked the action of noradrenaline but the beta-adrenergic agonist, isoproterenol, had no effect. In contrast to the duct cells, the endpiece cells responded to acetylcholine at much lower concentrations (threshold << 1 nmol/l) than to noradrenaline (threshold ca. 300 nmol/l) and the size of the increase in [Ca2+]i above resting levels evoked by acetylcholine (216 nmol/l) was nearly 5-times greater than for noradrenaline. VIP and substance P failed to evoke a Ca2+ response in either endpiece or duct cells.