Abstract：
: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-[beta-[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.
journal_name
Eur J Pharmacoljournal_title
European journal of pharmacologyauthors
Smaili SS,Cavalcanti PM,Oshiro ME,Ferreira AT,Jurkiewicz Adoi
10.1016/s0014-2999(97)01537-9subject
Has Abstractpub_date
1998-01-19 00:00:00pages
119-22issue
1eissn
0014-2999issn
1879-0712pii
S0014-2999(97)01537-9journal_volume
342pub_type
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