β1-Adrenoceptor-mediated relaxation with isoprenaline and the role of MaxiK channels in guinea-pig esophageal smooth muscle

• Published in: Journal of Smooth Muscle Research Vol. 40; no. 2; pp. 43 - 52
• Main Authors: Tanaka, Yoshio, Shinoda, Keiko, Sekiya, Sarasa, Yamaki, Fumiko, Shibano, Mari, Yamashita, Yoko, Horinouchi, Takahiro, Koike, Katsuo
• Format: Journal Article
• Language: English
• Published: Japan Society of Smooth Muscle Research 01.04.2004
• Subjects: esophageal smooth muscle; iberiotoxin; isoprenaline; large-conductance Ca2+-activated K+ (MaxiK) channels; β1-adrenoceptor
• ISSN: 0916-8737; 1884-8796
• DOI: 10.1540/jsmr.40.43

The possible functional coupling between β1-adrenoceptor and MaxiK channels which results in smooth muscle relaxation was examined in the guinea-pig esophageal muscularis mucosae. Isoprenaline-elicited relaxation of esophageal smooth muscle was confirmed to be mediated through β1-adrenoceptors as the response was competitively antagonized by a β1-selective antagonist atenolol with a pA2 value of 7.01. Iberiotoxin (IbTx, 10-7 M), a selective MaxiK channel inhibitor, substantially diminished the relaxant response to isoprenaline. The extent of the MaxiK channel contribution to the relaxant response was 15-40% of the control response when estimated as the E50%-Emax responses to isoprenaline. The relaxation to isoprenaline was also attenuated by high-KCl (80 mM) to the same degree as the relaxant response generated in the presence of IbTx, and thus the estimated extent of the K+ channel contribution was 10-40%. These findings indicate that β1-adrenoceptors are substantially coupled with MaxiK channels to produce relaxation of esophageal smooth muscle in the guinea-pig. Although MaxiK channels account for the contribution of K+ channels to the β1-adrenoceptor-mediated relaxation in this smooth muscle preparation, their contribution seems to be less when compared to the β2-adrenoceptor-mediated relaxation of tracheal smooth muscle.