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|Type:||Artigo de periódico|
|Title:||Modulation of Ca2+ and K+ permeabilities by oxotremorine-m (Oxo-m) in rodent pancreatic B-cells|
|Abstract:||The effects of the muscarinic agonist oxotremorine-m (Oxo-m) on Ca-45 and Rb-86 fluxes, insulin secretion, cytoplasmic Ca2+ concentration [Ca2+](i) and membrane potential in pancreatic B-cells were studied. Oxo-m (40-200 mu M) 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 mu M) increased the Ca-45 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 mu M) transiently increased Rb-86 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 (I-CRAC) is proposed to explain the sustained small changes in membrane potential.|
|Editor:||Cambridge Univ Press|
|Citation:||Experimental Physiology. Cambridge Univ Press, v. 82, n. 6, n. 967, n. 976, 1997.|
|Appears in Collections:||Unicamp - Artigos e Outros Documentos|
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