Lindström P, Norlund L, Sehlin J
Acta Physiol Scand. 1986 Dec;128(4):541-6. doi: 10.1111/j.1748-1716.1986.tb08010.x.
Potassium and chloride transport were measured in beta-cell-rich islets from ob/ob-mice using 36Cl- and 86Rb+ (K+-analogue). Reduction of the osmolarity from the normal 317 mosm l-1 to 180 mosm l-1 reduced the apparent content of K+ and Cl-. Hypo-osmolarity had no effect on the ouabain-sensitive portion of the Rb+ influx (Na+/K+ pump), but reduced the ouabain-resistant portion of the influx. Hypo-osmolarity also strongly increased the Rb+ efflux rate. Both tetracaine (0.5 mM) and glibenclamide (20 microM), which increase the osmotic resistance of pancreatic beta cells, significantly potentiated the reduction in apparent K+ content induced by hypo-osmolarity. This study suggests that the volume regulation in pancreatic beta cells is partly due to K+ and Cl- flux and that glibenclamide and tetracaine increase the osmotic resistance of the beta cells by affecting such ion transport.
使用³⁶Cl⁻和⁸⁶Rb⁺(钾离子类似物)测量ob/ob小鼠富含β细胞的胰岛中的钾离子和氯离子转运。渗透压从正常的317 mosm l⁻¹降低到180 mosm l⁻¹会降低钾离子和氯离子的表观含量。低渗对哇巴因敏感的铷离子内流部分(钠钾泵)没有影响,但会降低内流的哇巴因抵抗部分。低渗还会强烈增加铷离子外流速率。增加胰腺β细胞渗透压抗性的丁卡因(0.5 mM)和格列本脲(20 μM)均显著增强了低渗诱导的表观钾离子含量降低。这项研究表明,胰腺β细胞中的体积调节部分归因于钾离子和氯离子通量,并且格列本脲和丁卡因通过影响此类离子转运来增加β细胞的渗透压抗性。