Ozawa T
Department of Physiology, Tohoku University School of Medicine, Sendai, Japan.
Biochem Biophys Res Commun. 1998 May 19;246(2):422-5. doi: 10.1006/bbrc.1998.8636.
The effect of cAMP on a ryanodine-sensitive Ca2+ release from microsomal vesicles of rat parotid acinar cells was studied. After a steady state of ATP-dependent 45Ca2+ uptake into the vesicles, cAMP was added to the medium with thapsigargin (TG) to block a reuptake of 45Ca2+. The addition of cAMP (1.0 mM) with TG released about 10% of the 45Ca2+ that had been taken up. The cAMP-induced 45Ca2+ release was strongly inhibited by pretreatment of the vesicles with 500 microMM ryanodine. Preincubation with cAMP (1 mM) abolished ryanodine (10 microM)-induced 45Ca2+ release. The presence of a specific inhibitor of cAMP-dependent protein kinase (PKA) H-89 (10 microMM) inhibited the cAMP-induced 45Ca2+ release. These results indicate that in rat parotid acinar cells, cAMP can activate a ryanodine-sensitive Ca2+ release mechanism in the endoplasmic reticulum and that this activation is via a PKA-dependent process.
研究了环磷酸腺苷(cAMP)对大鼠腮腺腺泡细胞微粒体囊泡中对兰尼碱敏感的Ca2+释放的影响。在囊泡对ATP依赖的45Ca2+摄取达到稳态后,将cAMP与毒胡萝卜素(TG)加入培养基中以阻断45Ca2+的再摄取。cAMP(1.0 mM)与TG一起添加可释放出约10%已摄取的45Ca2+。用500微摩尔兰尼碱预处理囊泡可强烈抑制cAMP诱导的45Ca2+释放。用cAMP(1 mM)预孵育可消除兰尼碱(10微摩尔)诱导的45Ca2+释放。环磷酸腺苷依赖性蛋白激酶(PKA)的特异性抑制剂H-89(10微摩尔)的存在抑制了cAMP诱导的45Ca2+释放。这些结果表明,在大鼠腮腺腺泡细胞中,cAMP可激活内质网中对兰尼碱敏感的Ca2+释放机制,且这种激活是通过PKA依赖的过程实现的。