Effects of Ca2+ blockers on the various types of stimuli-induced acetylcholine release from guinea pig ileum myenteric plexus.
In the present study, we investigated the effects of various Ca2+ blockers on the release of acetylcholine (ACh) induced by nicotine, electrical field stimulation (EFS) and high-K+. Cd2+ markedly depressed the ACh release due to these stimuli. Verapamil inhibited the nicotine-induced ACh release remarkably and the EFS- or the high-K(+)-induced ACh release to a lesser extent. Since the nicotine- and the EFS-induced ACh releases were inhibited by procaine, the local anesthetic property of verapamil likely contributes in part to the inhibition. Diltiazem abolished the nicotine-induced ACh release completely but did not affect the EFS-induced release and significantly increased the high-K(+)-induced ACh release. These results suggest the absolute requirement for extracellular Ca2+ in the release of ACh induced by nicotine as well as EFS and high-K+. In addition, these stimuli may open the same Ca2+ channel to evoke ACh release.
Yokoyama
K
K
Department of Veterinary Pharmacology, College of Agriculture, University of Osaka Prefecture, Japan.
Yagasaki
O
O
D000109:Acetylcholine / Q000378:metabolism*; D000818:Animals; D002104:Cadmium / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D004558:Electric Stimulation; D006168:Guinea Pigs; D066298:In Vitro Techniques; D008297:Male; D009197:Myenteric Plexus / Q000187:drug effects / Q000378:metabolism* / Q000502:physiology; D009538:Nicotine / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology
D002121:Calcium Channel Blockers; D002104:Cadmium; D009538:Nicotine; D000109:Acetylcholine; D011188:Potassium