Abstract
Epinephrine caused a dose dependent increase in the electrical potential difference across the mouse parotid acinar cell membrane (hyperpolarization). Norepinephrine, synephrine and acetylcholine also caused membrane hyperpolarization. This hyperpolarization was not abolished by ouabain (1mm) and was enhanced in the absence of extracellular potassium. In constrast, the β-adrenoceptor agonist isoproterenol and its isomer metaproterenol caused membrane depolarization, this effect was blocked by propranolol (5 μm). In the presence of the α-adrenoceptor blocking agent phentolamine (10 μm), epinephrine stimulation also resulted in membrane depolarization while acetylcholine still hyperpolarized the cell membrane. The membrane effect of epinephrine (hyperpolarization) or isoproterenol (depolarization) was at least partly retained during superfusion of the parotid gland segments with Ca2+-free solution containing EGTA (10−4m) at a time when the resting membrane potential was reduced to 50% of its control value as a result of the extracellular Ca2+ deprivation.
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