Hashioka T
Department of Internal Medicine, School of Dentistry, Aichigakuin University, Nagoya, Japan.
Inflamm Res. 1995 Jun;44(6):245-7. doi: 10.1007/BF01782976.
The recepto-secretory mechanism in histamine-stimulated amylase release from rat parotid slices was studied using blockers of receptors and inhibitors of the intracellular messenger systems. Amylase release stimulated by histamine was inhibited by pyrilamine, an H1-receptor blocker, but not by cimetidine, an H2-receptor blocker. Atropine, prazosin and yohimbine had no effect on the release. Histamine-stimulated amylase release was inhibited by W-7, ML-9 and H-7, inhibitors of a calmodulin, a myosin light chain kinase (MLCK) and protein kinase C, respectively, while H-8, an inhibitor of protein kinase A, did not inhibit the release. These results suggest that histamine stimulation evokes amylase release via H1-receptors, followed by the Ca2+-dependent systems involving calmodulin, MLCK and protein kinase C.
利用受体阻断剂和细胞内信使系统抑制剂,研究了组胺刺激大鼠腮腺切片淀粉酶释放中的受体 - 分泌机制。组胺刺激引起的淀粉酶释放受到H1受体阻断剂吡苄明的抑制,但不受H2受体阻断剂西咪替丁的抑制。阿托品、哌唑嗪和育亨宾对释放无影响。组胺刺激的淀粉酶释放分别受到钙调蛋白抑制剂W - 7、肌球蛋白轻链激酶(MLCK)抑制剂ML - 9和蛋白激酶C抑制剂H - 7的抑制,而蛋白激酶A抑制剂H - 8则不抑制释放。这些结果表明,组胺刺激通过H1受体引发淀粉酶释放,随后是涉及钙调蛋白、MLCK和蛋白激酶C的Ca2 + 依赖性系统。