MLCK and PKC Involvements via Gi and Rho A Protein in Contraction by the Electrical Field Stimulation in Feline Esophageal Smooth Muscle.
10.4196/kjpp.2010.14.1.29
- Author:
Sun Young PARK
1
;
Jae Ho SHIM
;
Mina KIM
;
Yih Hsiu SUN
;
Hyun Soo KWAK
;
Xiangmei YAN
;
Byung Chul CHOI
;
Chaeuk IM
;
Sang Soo SIM
;
Ji Hoon JEONG
;
In Kyeom KIM
;
Young Sil MIN
;
Uy Dong SOHN
Author Information
1. College of Pharmacy, Chung-Ang University, Seoul 156-756, Korea. udsohn@cau.ac.kr
- Publication Type:Original Article
- Keywords:
Electrical field stimulation;
Smooth muscle;
Ca2+;
K+;
G protein;
On contraction;
Esophagus
- MeSH:
4-Aminopyridine;
Aluminum;
Aluminum Compounds;
Atropine;
Azepines;
Benzophenanthridines;
Contracts;
Esophagus;
Fluorides;
GTP-Binding Proteins;
Muscle, Smooth;
Myosin-Light-Chain Kinase;
NG-Nitroarginine Methyl Ester;
Nitric Oxide;
Pertussis Toxin;
Protein Kinase C;
rhoA GTP-Binding Protein;
Tetrodotoxin;
Transducers
- From:The Korean Journal of Physiology and Pharmacology
2010;14(1):29-35
- CountryRepublic of Korea
- Language:English
-
Abstract:
We have shown that myosin light chain kinase (MLCK) was required for the off-contraction in response to the electrical field stimulation (EFS) of feline esophageal smooth muscle. In this study, we investigated whether protein kinase C (PKC) may require the on-contraction in response to EFS using feline esophageal smooth muscle. The contractions were recorded using an isometric force transducer. On-contraction occurred in the presence of NG-nitro-L-arginine methyl ester (L-NAME), suggesting that nitric oxide acts as an inhibitory mediator in smooth muscle. The excitatory composition of both contractions was cholinergic dependent which was blocked by tetrodotoxin or atropine. The on-contraction was abolished in Ca2+-free buffer but reappeared in normal Ca2+-containing buffer indicating that the contraction was Ca2+ dependent. 4-aminopyridine (4-AP), voltage-dependent K+ channel blocker, significantly enhanced on-contraction. Aluminum fluoride (a G-protein activator) increased on-contraction. Pertussis toxin (a Gi inactivator) and C3 exoenzyme (a rhoA inactivator) significantly decreased on-contraction suggesting that Gi or rhoA protein may be related with Ca2+ and K+ channel. ML-9, a MLCK inhibitor, significantly inhibited on-contraction, and chelerythrine (PKC inhibitor) affected on the contraction. These results suggest that endogenous cholinergic contractions activated directly by low-frequency EFS may be mediated by Ca2+, and G proteins, such as Gi and rhoA, which resulted in the activation of MLCK, and PKC to produce the contraction in feline distal esophageal smooth muscle.
