The relationship between intracellular Ca2+ concentration and adrenergic agonist-induced amylase release in rat parotid acini

• Published in: Japanese Journal of Pharmacology 1990, Vol.52 (suppl-1.1), p.298-298
• Main Authors: Nomura, Hiroko, Yokoyama, Rie, Ukai, Kikuko, Nomura, Yukihiko, Chihara, Masaru, Tachibana, Masakatsu, Shigei, Tatsuro, Nomura, Takahide, Hagino, Yasumichi
• Format: Article
• Language: English
• ISSN: 0021-5198; 1347-3506
• DOI: 10.1016/S0021-5198(19)55716-X

It has been reported in the previous work that calcium(Ca) channel blockers potentiated dibutyryl cAMP(Bt_2 cAMP)-induced amylase release from rat parotid gland. Moreover, Ca channel blockers enhanced the potentiation of Bt_2 cAMP-induced amylase release by α-adrenergic agonists(methoxamine and clonidine). In the present study, 3 distinct Ca channel blockers(verapamil, diltiazem and nifedipine) were used to examine the relationship between the adrenergic agonist-induced rise in intracellular Ca^2+ concentration([Ca^2+ ]_i ) (measured by the Ca^2+ -sensitive fluorescent dye fura-2 AM) and amylase release in rat parotid acini. The basal [Ca^2+ ]_i in isolated parotid acini was 230-250 nM and this level decreased by 40-50 nM after the addition of Ca channel blockers. When Ca channel blockers and α-adrenergic agonists were simultaneously added to the cell suspension, there was no change in [Ca^2+ ]_i compared with the basal one. In the presence of both channel blockers and α-adrenergic agonist, isoproterenol or Bt_2 cAMP did not alter [Ca^2+ ]_i in parotid acini. These results revealed that there was significant dissociation between change in [Ca^2+ ]_i and the potentiation of isoproterenol- or Bt_2 cAMP-induced amylase release by α-adrenergic agonists.