Is calcium the final mediator of exocytosis in the rat parotid gland?
Rat parotid slices were partially depleted of cellular Ca by long (80-100 minute) incubations in media containing no added Ca and 5mM ethylene glycol bis(beta-aminoethyl ether)-N,N'-tetraacetic acid (EGTA). This treatment inhibited the secretory response (release of alpha-amylase) both to isoproterenol and to dibutyryl cyclic adenosine 3':5'-monophosphate. The isoproterenol-stimulated synthesis of cyclic adenosine 3':5'-monophosphate was inhibited by depletion of Ca but not to an extent sufficient to explain the effects of depletion of Ca on secretion. Isoproterenol did not affect influx of 45Ca but stimulated efflux of 45Ca suggesting release of Ca from intracellular stores. Isoproterenol caused vacuolation of the Golgi region and (in high concentration) enhanced the release of 86Rb, responses which are both believed to be mediated by an increase in cytoplasmic Ca concentration. The results of these experiments suggest that isoproterenol acts to increase the tissue level of cyclic adenosine 3':5'-monophosphate which in turn acts to release Ca from intracellular stores. The rise in intracellular Ca concentration is believed to mediate exocytosis.
D000818:Animals; D003994:Bucladesine / Q000494:pharmacology; D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium / Q000502:physiology*; D002217:Carbachol / Q000494:pharmacology; D005089:Exocytosis / Q000187:drug effects; D066298:In Vitro Techniques; D007545:Isoproterenol / Q000494:pharmacology; D008274:Magnesium / Q000502:physiology; D010306:Parotid Gland / Q000502:physiology*; D010656:Phenylephrine / Q000494:pharmacology; D011188:Potassium / Q000502:physiology; D051381:Rats
D010656:Phenylephrine; D000001:Calcimycin; D003994:Bucladesine; D002217:Carbachol; D008274:Magnesium; D007545:Isoproterenol; D011188:Potassium; D002118:Calcium