Calcium and energy requirements for K + release mediated by the epinephrine -receptor in rat parotid slices.
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Acetates↗
Biomedical subjects
S Batzri
Publications and source records attributed to S Batzri.
Pseudopodia formation by secretory granules.
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Adenosine Triphosphate↗
Potassium ion release and enzyme secretion: adrenergic regulation by alpha- and beta-receptors.
Epinephrine caused amylase secretion and K(+) release in rat parotid slices. Propranolol, which blocks beta-receptors, inhibited amylase secretion; phentolamine, which blocks alpha-receptors, inhibited K(+) release. Since enzyme secretion was associated with fusion of secretory granules to the cell membrane and K(+) release was associated with vacuole formation, it could be shown that both alpha- and beta-receptors are present in the same exocrine cell. The findings appear to exclude cyclic 3',5'-adenosine monophosphate as an intermediate in the alpha-receptor response.
Adrenergic alpha-Antagonists↗
Epinephrine-induced vacuole formation in parotid gland cells and its independence of the secretory process.
Catecholamines cause rapid release of K(+) and formation of vacuoles in acinar gland cells. A high K(+) concentration in the medium bathing parotid gland slices prevents vacuole formation by epinephrine and facilitates the secretion of most of the exportable amylase. N(6)-monobutyryl 3':5'-cyclic AMP does not cause K(+) release and vacuole formation although it efficiently induces amylase secretion. It is suggested that the secretory process is independent of vacuole formation.
Amylases↗