Tohmatsu T, Nishida A, Nagao S, Nakashima S, Nozawa Y
Department of Biochemistry, Gifu University School of Medicine, Japan.
Biochim Biophys Acta. 1989 Sep 19;1013(2):190-3. doi: 10.1016/0167-4889(89)90048-7.
Ca2+ release triggered by inositol 1,4,5-trisphosphate (IP3) has been measured in saponin-permeabilized human platelets with quin2 or 45Ca2+. Ca2+ was sequestered by intracellular organelles in the presence of ATP, and IP3 released half of the sequestered Ca2+. The addition of cyclic AMP (cAMP) to permeabilized platelets transiently accelerated Ca2+ sequestration, but did not alter the steady-state level. In contrast, IP3-induced Ca2+ release was greatly inhibited by cAMP. Phorbol myristate acetate, an activator of protein kinase C did not affect IP3-induced Ca2+ release. These results indicate that cAMP may be involved in the regulation of IP3-induced Ca2+ release in human platelets.
利用喹啉2或45Ca2+，在皂角苷通透的人血小板中测量了由肌醇1,4,5 -三磷酸（IP3）触发的Ca2+释放。在ATP存在的情况下，Ca2+被细胞内细胞器螯合，IP3释放了一半被螯合的Ca2+。向通透的血小板中添加环磷酸腺苷（cAMP）可短暂加速Ca2+螯合，但不改变稳态水平。相比之下，cAMP可极大地抑制IP3诱导的Ca2+释放。佛波醇肉豆蔻酸酯乙酸盐，一种蛋白激酶C激活剂，不影响IP3诱导的Ca2+释放。这些结果表明，cAMP可能参与了人血小板中IP3诱导的Ca2+释放的调节。
