Ca2+ release-activated channels in rat stomach smooth muscle cells
Autor: | Paulo M. Cavalcanti, Soraya S. Smaili, Maria E.M. Oshiro, Alice T. Ferreira, Aron Jurkiewicz |
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Rok vydání: | 1998 |
Předmět: |
medicine.medical_specialty
Thapsigargin chemistry.chemical_element In Vitro Techniques Calcium Calcium in biology chemistry.chemical_compound Internal medicine medicine Animals Gastric Fundus Rats Wistar Pharmacology Isradipine Chemistry Antagonist T-type calcium channel Muscle Smooth Long-term potentiation Rats Endocrinology Biophysics Calcium Channels medicine.symptom Muscle Contraction Muscle contraction medicine.drug |
Zdroj: | European Journal of Pharmacology. 342:119-122 |
ISSN: | 0014-2999 |
DOI: | 10.1016/s0014-2999(97)01537-9 |
Popis: | In rat stomach fundus, contractions induced by Ca 2+ (1.8 mM) were strikingly potentiated by thapsigargin. This potentiation was partially inhibited by the blockers of Ca 2+ 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 Ca 2+ . 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. |
Databáze: | OpenAIRE |
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