Whole gland perfusion technique was applied to rat parotid glands to assess whether amylase affects fluid secretion. Control perfusion without any secretagogue evoked no spontaneous secretion. Carbachol (CCh 1 microM) induced both amylase and fluid secretion with distinctive kinetics. Fluid secretion occurred constantly around 60 microL/g-min, whereas amylase secretion exhibited an initial peak, followed by a rapid decrease to reach a plateau. Isoproterenol (Isop 1 microM) alone did not induce fluid secretion although it evoked amylase secretion as measured in isolated perfused acini. Addition of Isop during CCh stimulation evoked a rapid and large rise in amylase secretion accompanied by small increase in oxygen consumption. Morphological observations carried out by HR SEM and TEM revealed exocytotic profiles following Isop stimulation. CCh stimulation alone seldom showed exocytotic profiles, suggesting a low incidence of amylase secretion during copious fluid secretion. Combined stimulation of CCh and Isop induced both vacuolation and exocytosis along intercellular canaliculi. These findings suggest that control of salivary fluid secretion is independent of the amylase secretion system induced by CCh and/or Isop.
Amylases/metabolism* ; Animal ; Carbachol/pharmacology ; Cholinergic Agonists/pharmacology ; In Vitro ; Isoproterenol/pharmacology ; Male ; Microscopy, Electron ; Microscopy, Electron, Scanning ; Oxygen Consumption/physiology ; Oxygen Consumption/drug effects ; Parotid Gland/ultrastructure ; Parotid Gland/secretion* ; Parotid Gland/enzymology* ; Perfusion ; Rats ; Rats, Wistar ; Saliva/metabolism* ; Sympathomimetics/pharmacology

Receptor- and nonreceptor-mediated stimuli produce increases in both PKCdelta tyrosine phosphorylation and activity in rat parotid acinar cells and other cells. In vivo and in vitro increases and decreases in tyrosine phosphorylation resulted in increases and decreases, respectively, of PKCdelta activity. These studies demonstrated that increases in PKCdelta activity by G protein-coupled receptors and other stimuli were controlled by alterations in tyrosine phosphorylation.
Animal ; Enzyme Activation/physiology ; Isoenzymes/metabolism* ; Male ; Parotid Gland/enzymology* ; Phosphorylation ; Protein Kinase C/metabolism* ; Rats ; Rats, Sprague-Dawley ; Tyrosine/metabolism*