Cui Z J
Beijing Agricultural University, Faculty of Biological Sciences, China.
Zhongguo Yao Li Xue Bao. 1997 May;18(3):255-8.
To study whether M3 receptor occupation would lead to activation of calcium/calmodulin-dependent protein kinase II (CaM kinase II).
In this study, we isolated rat pancreatic acini by collagenase digestion; measured the Ca2+/calmodulin-independent activity of autophosphorylated form of the CaM kinase II both before and after stimulation of the acini with muscarinic secretagogue bethanechol (Bet).
Bet stimulated the activation of, or generation of Ca(2+)-independent activity of, this kinase, in a concentration (0.0001-1 mmol.L-1) and time (5-300 s)-dependent manner; with Bet of 100 mumol.L-1, Ca(2+)-independent activity increased from an unstimulated level of 4.5 +/- 0.3 (n = 4) to 8.9 +/- 1.3 (n = 4, P < 0.05) at 5 s. Another Ca2+ mobilizing secretagogue cholecystokinin (CCK) also activated the kinase; at 1 mumol.L-1, CCK increased Ca(2+)-independent kinase activity to 12.9 +/- 0.5 (n = 6, P < 0.05). Vasoactive intestinal peptide (VIP) at 1 mumol.L-1 did not produce significant Ca(2+)-independent kinase activity (from control 3.90 +/- 0.28 to 4.53 +/- 0.47, n = 6, P > 0.05). Atropine completely blocked Bet activation of the kinase.
CaM kinase II plays a pivotal role in digestive enzyme secretion, especially during the initial phase of amylase secretion.
研究M3受体被占据是否会导致钙/钙调蛋白依赖性蛋白激酶II（CaM激酶II）的激活。
在本研究中，我们通过胶原酶消化分离大鼠胰腺腺泡；在用毒蕈碱促分泌剂氨甲酰甲胆碱（Bet）刺激腺泡前后，测量CaM激酶II自磷酸化形式的钙/钙调蛋白非依赖性活性。
Bet以浓度（0.0001 - 1 mmol·L-1）和时间（5 - 300秒）依赖性方式刺激该激酶的激活或产生钙非依赖性活性；在100 μmol·L-1的Bet作用下，5秒时钙非依赖性活性从未刺激水平的4.5±0.3（n = 4）增加到8.9±1.3（n = 4，P < 0.05）。另一种钙动员促分泌剂胆囊收缩素（CCK）也激活了该激酶；在1 μmol·L-1时，CCK将钙非依赖性激酶活性增加到12.9±0.5（n = 6，P < 0.05）。1 μmol·L-1的血管活性肠肽（VIP）未产生显著的钙非依赖性激酶活性（从对照的3.90±0.28增加到4.53±0.47，n = 6，P > 0.05）。阿托品完全阻断了Bet对该激酶的激活。
CaM激酶II在消化酶分泌中起关键作用，尤其是在淀粉酶分泌的初始阶段。
