On stimulating receptors(muscarinic, substance P) in plasma membrane of the salivary gland, the elevation of cytosolic calcium (Ca2+) evokes the salivary secretion. There are two basic mechanisms of Ca2+ mobilization by which the cell increase its cytosolic free calcium : 1) via Ca2+ release triggered by inositol trisphosphate (IP3), and 2) via entry of extracellular Ca2+. In addition, there are several possibilities by which intracellular Ca2+ concentration may be modulated by the IP3-insensitive Ca2+ pool (IICP) and intracellular Ca2+ mobilization might be sophisticately intercommunicated with types of agonists and the interaction among agonists. This study was aimed at characterizing the Ca2+ mobilization system of rat parotid glands in resonse to carbachol (CCH) and substance P (Sub-P). The minced tissue of rat parotid acini was placed in the perifusion chamber with the K+-sensitive electrode(Orion Research), followed by perfusing the Krebs-Ringer bicarbonate solution. In order to stimulate the parotid acini, CCh and Sub-P were perfused with KRB solution. Also, the K+-release from parotid acini was measured and interpreted in terms of the intracellular Ca2+ concentration. In the absence of Ca2+ the parotid acini was repeatedly stimulated by CCh. As a result, CCh induced K+-release was dramatically reduced. However, the addition of Ca2+ caused an increase in the CCh-induced K+-release. On the other hand, staurosporine(10-6 M). an inhibitor of PKC, did not affect the CCh-induced K+-release. A dose of 10 mM caffeine
given to parotid acini increased the K+-release in both cases of Ca2+, and Ca2+ free solution. But the level of K+-release was sustained higher in the presence of Ca2+. In addition, parotid acini were stimulated by the CCh under the condition of
caffeine pretreatment. Consequently, CCh-induced K+-release was remarkably inhibited in the presence or absence of Ca2+, while Sub-P-induced K+-release was not changed by the caffeine pretreatment. Nevertheless. If CCh or Sub-P was administrated with caffeine at a time, caffeine did not blunt the CCh-induced K+-release. Furthermore, the removal of caffeine in the sustained phase resulted in the successive increase of K+-release by the CCh, while not in the case of Sub-P. Taken all together, CCh- and Sub-P-induced K+ -release seem to be caused by Ca2+ entry and the cytosolic Ca2+ released from internal Ca2+ store. However, the regulation of Ca2+ mobilization of sub-P might be different from that of CCh. In particular, the process of Ca2+ entry may be closely associated with the filling state of internal Ca2+ store. However, the interrelation between Ca2+ entry and internal Ca2+ store in terms of Ca2+ mobilization, should be remained to be solved.
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