Competitive antagonism by glibenclamide of cromakalim inhibition of twitch contractions in rabbit vas deferens

Electrically induced contractions of the rabbit isolated vas deferens were potentiated by carbachol but inhibited by the K+ channel opener cromakalim. The inhibition by cromakalim could be competitively antagonized by 10(-7)-10(-6) M glibenclamide (pA2 = 7.17) and was also reversed by carbachol, ext...

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Bibliographic Details
Published inEuropean journal of pharmacology Vol. 161; no. 1; p. 103
Main Author Eltze, M
Format Journal Article
LanguageEnglish
Published Netherlands 14.02.1989
Subjects
3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester - pharmacology
Animals
Benzopyrans - antagonists & inhibitors
Benzopyrans - pharmacology
Calcium Channel Blockers - pharmacology
Cromakalim
Electric Stimulation
Glyburide - pharmacology
In Vitro Techniques
Male
Muscle, Smooth - drug effects
Potassium Channels - drug effects
Pyrroles - antagonists & inhibitors
Pyrroles - pharmacology
Rabbits
Vas Deferens - drug effects
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Summary:Electrically induced contractions of the rabbit isolated vas deferens were potentiated by carbachol but inhibited by the K+ channel opener cromakalim. The inhibition by cromakalim could be competitively antagonized by 10(-7)-10(-6) M glibenclamide (pA2 = 7.17) and was also reversed by carbachol, extra K+ or Bay k 8644. The data support the view that smooth muscle membrane depolarization is the cause for carbachol potentiation in rabbit vas deferens and that hyperpolarization by cromakalim is susceptible to blockade by the inhibitor of ATP-sensitive K+ channels, glibenclamide.
ISSN:0014-2999
DOI:10.1016/0014-2999(89)90187-8