Wilson S M, Ko W H, Pediani J D, Rakhit S, Nichol J A, Bovell D L
Institute of Physiology, University of Glasgow, U.K.
Comp Biochem Physiol A Physiol. 1995 Jun;111(2):215-21. doi: 10.1016/0300-9629(95)00011-u.
We measured the rates of 125I- and 86Rb+ efflux from preloaded, cultured equine sweat gland cells. The calcium ionophore ionomycin increased the efflux of both isotopes. Anion efflux was unaffected by Ba2+, but this cation inhibited 86Rb(+)-efflux, suggesting that [Ca2+]i-activated potassium channels were present. Activation of these channels was not, however, important for the efflux of anions. We measured 125I- efflux from valinomycin-depolarised cells in which anion cotransport was inhibited. Changes in 125I- efflux reflect changes in anion permeability under these conditions, and ionomycin caused a clear permeability increase that was abolished by the anion channel blocker diphenylamine-2-carboxylate. ATP and UTP increased the efflux of both isotopes, suggesting that type P2U purine receptors allow these nucleotides to regulate membrane permeability.
我们测量了预加载的培养马汗腺细胞中(^{125}I)和(^{86}Rb^+)的流出速率。钙离子载体离子霉素增加了两种同位素的流出。阴离子流出不受(Ba^{2 +})影响,但这种阳离子抑制了(^{86}Rb^+)的流出,表明存在[Ca²⁺]i激活的钾通道。然而,这些通道的激活对阴离子流出并不重要。我们测量了缬氨霉素去极化细胞中(^{125}I)的流出,其中阴离子共转运受到抑制。在这些条件下,(^{125}I)流出的变化反映了阴离子通透性的变化,离子霉素导致通透性明显增加,而这种增加被阴离子通道阻滞剂二苯胺-2-羧酸盐消除。ATP和UTP增加了两种同位素的流出,表明P2U型嘌呤受体允许这些核苷酸调节膜通透性。