McNulty T J, Taylor C W
Department of Pharmacology, University of Cambridge, U.K.
Biochem J. 1993 May 1;291 ( Pt 3)(Pt 3):799-801. doi: 10.1042/bj2910799.
Caffeine has been much used to examine the possibility that ryanodine receptors similar to those found in skeletal and cardiac muscle may be more widely distributed and perhaps contribute to regenerative Ca2+ signals in electrically inexcitable cells. In permeabilized hepatocytes loaded with 45Ca2+, caffeine (> or = 5 mM) decreased the 45Ca2+ content of the intracellular stores by up to 60%; the effect was substantially reversible and it was not mimicked by the closely related methylxanthine theophylline (20 mM). Ryanodine (5 microM) stimulated a far smaller Ca2+ mobilization (7 +/- 1%). Procaine (1 mM), Ruthenium Red (10 microM) and ryanodine (5 microM) did not affect the Ca2+ release evoked by InsP3 (3 microM) or caffeine (30 mM). We conclude that caffeine can specifically cause Ca2+ release from the intracellular stores of hepatocytes, but the effect is unlikely to be mediated by ryanodine receptors.
即类似于在骨骼肌和心肌中发现的兰尼碱受体可能分布更为广泛，并且或许有助于电惰性细胞中的Ca2+再生信号。在用45Ca2+加载的通透化肝细胞中，咖啡因（≥5 mM）可使细胞内储存库中的45Ca2+含量降低多达60%；该效应基本可逆，且与之密切相关的甲基黄嘌呤茶碱（20 mM）无法模拟此效应。兰尼碱（5 μM）刺激的Ca2+动员要小得多（7±1%）。普鲁卡因（1 mM）、钌红（10 μM）和兰尼碱（5 μM）不影响由肌醇三磷酸（3 μM）或咖啡因（30 mM）诱发的Ca2+释放。我们得出结论，咖啡因可特异性地引起肝细胞内储存库中的Ca2+释放，但这种效应不太可能由兰尼碱受体介导。
