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

• Published in: European journal of pharmacology Vol. 342; no. 1; pp. 119 - 122
• Main Authors: Smaili, Soraya S, Cavalcanti, Paulo M, Oshiro, Maria Etsuko M, Ferreira, Alice T, Jurkiewicz, Aron
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier B.V 19.01.1998; Elsevier
• 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; Thapsigargin; Calcium store; SK&F96365; Isradipine; Miconazole; Stomach fundus, rat; Stomach; Rat; Digestive system; Rodentia; Smooth muscle; Ionic channel; Muscle contraction; In vitro; Vertebrata; Mammalia; Calcium ion; Animal; Ionic movement
• ISSN: 0014-2999; 1879-0712
• DOI: 10.1016/S0014-2999(97)01537-9

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.