| dc.creator | Bordin, S | |
| dc.creator | Carneiro, EM | |
| dc.creator | Boschero, AC | |
| dc.date | 1997 | |
| dc.date | NOV | |
| dc.date | 2014-12-16T11:37:31Z | |
| dc.date | 2015-11-26T16:26:33Z | |
| dc.date | 2014-12-16T11:37:31Z | |
| dc.date | 2015-11-26T16:26:33Z | |
| dc.date.accessioned | 2018-03-28T23:07:21Z | |
| dc.date.available | 2018-03-28T23:07:21Z | |
| dc.identifier | Experimental Physiology. Cambridge Univ Press, v. 82, n. 6, n. 967, n. 976, 1997. | |
| dc.identifier | 0958-0670 | |
| dc.identifier | WOS:A1997YJ00700002 | |
| dc.identifier | http://www.repositorio.unicamp.br/jspui/handle/REPOSIP/57682 | |
| dc.identifier | http://www.repositorio.unicamp.br/handle/REPOSIP/57682 | |
| dc.identifier | http://repositorio.unicamp.br/jspui/handle/REPOSIP/57682 | |
| dc.identifier.uri | http://repositorioslatinoamericanos.uchile.cl/handle/2250/1268925 | |
| dc.description | 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. | |
| dc.description | 82 | |
| dc.description | 6 | |
| dc.description | 967 | |
| dc.description | 976 | |
| dc.language | en | |
| dc.publisher | Cambridge Univ Press | |
| dc.publisher | New York | |
| dc.relation | Experimental Physiology | |
| dc.relation | Exp. Physiol. | |
| dc.rights | fechado | |
| dc.rights | http://journals.cambridge.org/action/displaySpecialPage?pageId=4676 | |
| dc.source | Web of Science | |
| dc.subject | Induced Insulin Release | |
| dc.subject | Cytosolic-free Calcium | |
| dc.subject | Beta-cells | |
| dc.subject | Intracellular Calcium | |
| dc.subject | Muscarinic Receptors | |
| dc.subject | Electrical-activity | |
| dc.subject | Mouse Islets | |
| dc.subject | Glucose | |
| dc.subject | Acetylcholine | |
| dc.subject | Secretion | |
| dc.title | Modulation of Ca2+ and K+ permeabilities by oxotremorine-m (Oxo-m) in rodent pancreatic B-cells | |
| dc.type | Artículos de revistas | |
