The Influences of G Proteins, Ca2+, and K+ Channels on Electrical Field Stimulation in Cat Esophageal Smooth Muscle.
10.4196/kjpp.2009.13.5.393
- Author:
Jun Hong PARK
1
;
Hyun Sik KIM
;
Sun Young PARK
;
Chaeuk IM
;
Ji Hoon JEONG
;
In Kyeom KIM
;
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:
EFS;
Cat esophageal;
Circular smooth muscle;
NO;
L-type Ca2+ channel
- MeSH:
Animals;
Atropine;
Cats;
Cholera Toxin;
Contracts;
GTP-Binding Protein alpha Subunits;
GTP-Binding Proteins;
Ion Channels;
Muscle, Smooth;
Muscles;
Neurons;
NG-Nitroarginine Methyl Ester;
Nimodipine;
Nitric Oxide Synthase;
Pertussis Toxin;
Phospholipases;
Pinacidil;
Proteins;
Tetraethylammonium;
Tetrodotoxin
- From:The Korean Journal of Physiology and Pharmacology
2009;13(5):393-400
- CountryRepublic of Korea
- Language:English
-
Abstract:
NO released by myenteric neurons controls the off contraction induced by electrical field stimulation (EFS) in distal esophageal smooth muscle, but in the presence of nitric oxide synthase (NOS) inhibitor, L-NAME, contraction by EFS occurs at the same time. The authors investigated the intracellular signaling pathways related with G protein and ionic channel EFS-induced contraction using cat esophageal muscles. EFS-induced contractions were significantly suppressed by tetrodotoxin (1 micrometer) and atropine (1 micrometer). Furthermore, nimodipine inhibited both on and off contractions by EFS in a concentration dependent meaner. The characteristics of 'on' and 'off' contraction and the effects of G-proteins, phospholipase, and K+ channel on EFS-induced contraction in smooth muscle were also investigated. Pertussis toxin (PTX, a Gi inactivator) attenuated both EFS-induced contractions. Cholera toxin (CTX, Gs inactivator) also decreased the amplitudes of EFS-induced off and on contractions. However, phospholipase inhibitors did not affect these contractions. Pinacidil (a K+ channel opener) decreased these contractions, and tetraethylammonium (TEA, K+ Ca channel blocker) increased them. These results suggest that EFS-induced on and off contractions can be mediated by the activations Gi or Gs proteins, and that L-type Ca2+ channel may be activated by G-protein alpha subunits. Furthermore, K+ Ca-channel involve in the depolarization of esophageal smooth muscle. Further studies are required to characterize the physiological regulation of Ca2+ channel and to investigate the effects of other K+ channels on EFS-induced on and off contractions.
