Habuchi Y, Tanaka H, Yamamoto T, Nishio M, Morikawa J, Yoshimura M
Department of Laboratory Medicine, Kyoto Prefectural University of Medicine, Japan.
Can J Cardiol. 1997 Dec;13(12):1188-90.
Effects of acetylcholine (ACh) on the L-type calcium current were examined in isolated atrioventricular nodal cells that exhibited spontaneous contractions. ACh (0.1 to 10 microM) inhibited basal calcium current dose-dependently. This inhibition was eliminated by dialysis with 8Br cAMP or cAMP-dependent kinase inhibitory peptide. Both extracellular N-ethylmaleimide 50 microM and intracellular GDPssS 0.2 mM abolished the ACh effect. Dialysis with cGMP or NG-monomethyl-L-arginine did not significantly affect ACh inhibition of basal calcium current. Similarly, cGMP-dependent protein kinase inhibitor KT5823 (1 microM) and the type II phosphodiesterase inhibitor erythro-9-(2-hydroxy-3-nonyl) adenine (30 microM) did not attenuate the ACh effect. Therefore, ACh inhibits the basal calcium current in the atrioventricular node mainly by suppressing cAMP synthesis through the inhibitory GTP-binding protein.
在表现出自发收缩的离体房室结细胞中，研究了乙酰胆碱（ACh）对L型钙电流的影响。ACh（0.1至10微摩尔）剂量依赖性地抑制基础钙电流。用8Br cAMP或cAMP依赖性激酶抑制肽进行透析可消除这种抑制作用。细胞外50微摩尔N-乙基马来酰亚胺和细胞内0.2毫摩尔GDPssS均消除了ACh的作用。用cGMP或NG-单甲基-L-精氨酸进行透析对ACh抑制基础钙电流没有显著影响。同样，cGMP依赖性蛋白激酶抑制剂KT5823（1微摩尔）和II型磷酸二酯酶抑制剂erythro-9-（2-羟基-3-壬基）腺嘌呤（30微摩尔）也没有减弱ACh的作用。因此，ACh主要通过抑制性GTP结合蛋白抑制cAMP合成来抑制房室结中的基础钙电流。
