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Modulation of Ca2+ and K+ permeabilities by oxotremorine‐m (Oxo‐m) in rodent pancreatic B‐cells
Author(s) -
Bordin S,
Carneiro EM,
Boschero AC
Publication year - 1997
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.1997.sp004082
Subject(s) - oxotremorine , rodent , chemistry , modulation (music) , biophysics , endocrinology , medicine , biology , biochemistry , physics , receptor , muscarinic acetylcholine receptor , ecology , acoustics
The effects of the muscarinic agonist oxotremorine‐m (Oxo‐m) on 45Ca and 86Rb fluxes, insulin secretion, cytoplasmic Ca2+ concentration ([Ca2+]i) and membrane potential in pancreatic B‐cells were studied. Oxo‐m (40–200 microM) increased the [Ca2+]i by about 250 nM, irrespective of the glucose concentration present in the medium (2.8–22 mM). This effect was reduced by 50% upon the addition of EGTA. Oxo‐m (50 microM) increased the 45Ca efflux from islets perifused in the absence or presence of [Ca2+]o, although under the former condition this efflux was transient. The difference between effluxes measured in the absence and presence of [Ca2+]o represents the sustained second component, which presumably reflects Ca2+ influx. In both the absence and presence of 11.2 mM glucose. Oxo‐m (50 microM) transiently increased 86Rb efflux. In the presence of glucose, Oxo‐m provoked a transient polarization of the B‐cell membrane associated with an increase in the K+ permeability values. K+ permeability returned to basal values (no Oxo‐m) after 1–2 min. These results indicate that the initial phase of Oxo‐m‐induced insulin secretion depends partially on intracellular Ca2+ release, and that the sustained enhancement of release depends on Ca2+ influx. The participation of a calcium release‐activated current (ICRAC) is proposed to explain the sustained small changes in membrane potential.