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Effects of Ca2+ channel agonist‐antagonist enantiomers of dihydropyridine 202791 on insulin release, 45Ca uptake and electrical activity in isolated pancreatic islets
Author(s) -
Boschero AC,
Carroll PB,
De Souza C,
Atwater I
Publication year - 1990
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.1990.sp003431
Subject(s) - dihydropyridine , endocrinology , agonist , medicine , antagonist , pancreatic islets , chemistry , insulin , islet , calcium , receptor , biology
This is the first study using the selective agonist/antagonist stereoisomers of dihydropyridine 202791 to investigate stimulus‐secretion coupling in pancreatic islet cells. We studied effects of the (+)(Ca2+ channel agonist) and (‐)(Ca2+ channel antagonist) forms of the dihydropyridine, on 45calcium net uptake, insulin secretion, and membrane potential measured in rodent islets. The antagonist partially inhibited glucose‐induced insulin secretion and Ca2+ uptake; however, the potassium‐induced Ca2+ uptake was completely inhibited. The antagonist did not completely block glucose‐evoked spike activity. Addition of the agonist enhanced insulin release and Ca2+ uptake in the presence of 5.6 mM‐glucose, but did not increase insulin release or Ca2+ uptake in 16.7 mM‐glucose. In the presence of tetraethylammonium (TEA), (+)202791 increased and (‐)202791 decreased the duration of glucose‐induced action potentials. The results again confirm the presence of a dihydropyridine‐sensitive Ca2+ channel in pancreatic B‐cells. In addition these data suggest that in these cells there is activation of a dihydropyridine‐insensitive Ca2+ entry in the presence of glucose.