Ca2+ release-activated channels in rat stomach smooth muscle cells

In rat stomach fundus, contractions induced by Ca2+ (1.8 mM) were strikingly potentiated by thapsigargin. This potentiation was partially inhibited by the blockers of Ca2+ release activated channels (CRACs), miconazole and SK&F96365 ({1-[β-[3-(4-methoxyphenyl)propoxy]-4-methoxyphenethyl]-1H-imid...

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Bibliographic Details
Published in:European journal of pharmacology 1998-01, Vol.342 (1), p.119-122
Main Authors: Smaili, Soraya S, Cavalcanti, Paulo M, Oshiro, Maria Etsuko M, Ferreira, Alice T, Jurkiewicz, Aron
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Calcium - metabolism
Calcium Channels - metabolism
Calcium store
Fundamental and applied biological sciences. Psychology
Gastric Fundus - cytology
Gastric Fundus - metabolism
In Vitro Techniques
Isradipine
Miconazole
Muscle Contraction - physiology
Muscle, Smooth - cytology
Muscle, Smooth - metabolism
Rats
Rats, Wistar
SK&F96365
Stomach
Stomach fundus, rat
Thapsigargin
Vertebrates: digestive system
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Summary:In rat stomach fundus, contractions induced by Ca2+ (1.8 mM) were strikingly potentiated by thapsigargin. This potentiation was partially inhibited by the blockers of Ca2+ release activated channels (CRACs), miconazole and SK&F96365 ({1-[β-[3-(4-methoxyphenyl)propoxy]-4-methoxyphenethyl]-1H-imidazole, HCL}) and slightly blocked by the antagonist of calcium voltage-operated channels (VOCs), isradipine. In dissociated cells in a 0Ca solution, thapsigargin potentiated the increase in intracellular calcium after reintroduction of Ca2+. This potentiation was partially reduced by the CRAC blockers, but not by the VOC blockers. This data suggests that calcium influx increased due to the depletion of intracellular calcium by thapsigargin and that this influx occurs predominantly through CRACs.
ISSN:0014-2999
1879-0712
DOI:10.1016/S0014-2999(97)01537-9