Effects of endothelin-1 on the membrane potential and slow waves in circular smooth muscle of rat gastric antrum

• Published in: Journal of Smooth Muscle Research Vol. 40; no. 4,5; pp. 199 - 210
• Main Authors: Imaeda, Kenro, Kato, Takashi, Okayama, Naotsuka, Imai, Seiji, Sasaki, Makoto, Kataoka, Hiromi, Nakazawa, Takahiro, Ohara, Hirotaka, Kito, Yoshihiko, Itoh, Makoto
• Format: Journal Article
• Language: English
• Published: Japan Japan Society of Smooth Muscle Research 2004
• Subjects: 4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid - pharmacology; Action Potentials - drug effects; Action Potentials - physiology; Animals; Apamin - pharmacology; Ca2+-activated K+ channel; Electromyography; Endothelin-1 - pharmacology; endothelin-1 receptor; gastric smooth muscle; Male; membrane potential; Muscle, Smooth - drug effects; Muscle, Smooth - physiology; Potassium Channels, Calcium-Activated - physiology; Pyloric Antrum - drug effects; Pyloric Antrum - physiology; Rats; Receptor, Endothelin A - physiology; Receptor, Endothelin B - physiology; slow wave
• ISSN: 0916-8737; 1884-8796
• DOI: 10.1540/jsmr.40.199

Electrophysiological effects of endothelin-1 (ET-1) on circular smooth muscle of rat gastric antrum were investigated by using intracellular membrane potential recording techniques. ET-1 (10 nM) caused an initial hyperpolarization of the membrane which was followed by a sustained depolarization. ET-1 also increased the frequency but not the amplitude of slow waves. In the presence of the endothelin type A (ETA) receptor antagonist, BQ123 (1 μM), ET-1 (10 nM) depolarized the membrane and increased the frequency of slow waves, but without the initial hyperpolarization. The selective endothelin type B (ETB) receptor agonist, sarafotoxin S6c (10 nM), also depolarized the membrane and increased the frequency of slow waves. In the presence of the ETB receptor antagonist, BQ788 (1 μM), ET-1 (10 nM) hyperpolarized the membrane. However, in the presence of BQ788, ET-1 caused neither the depolarization nor the increase in the frequency of the slow waves. The ET-1-induced hyperpolarization was completely abolished by apamin (0.1 μM). In the presence of apamin, ET-1 depolarized the membrane and increased the frequency of slow waves. The ET-1-induced depolarization was significantly attenuated by 4,4'-diisothiocyanatostilbene-2,2'-disulphonic acid (DIDS, 0.3 mM). The increase of the frequency by ET-1 was observed both in the presence and absence of DIDS. These results suggest that, ET-1 hyperpolarizes the membrane by the activation of Ca2+-activated K+ channels via ETA receptors, and depolarizes the membrane by the activation of Ca2+-activated Cl- channels via ETB receptors. ET-1 also appears to increase the frequency of slow waves via ETB receptors, however this mechanism would seem to be independent of membrane depolarization.