Rückes C, Blank U, Möller K, Rieboldt J, Lindemann H, Münker G, Clauss W, Weber W M
CF Working Group Giessen, Justus-Liebig-University, Germany.
Biochem Biophys Res Commun. 1997 Aug 28;237(3):488-91. doi: 10.1006/bbrc.1997.7106.
We characterized Na+ absorption in confluent monolayers of primary cultured epithelia derived from human nasal cystic fibrosis (CF) and non-CF epithelium in modified Ussing chambers. Amiloride-sensitive Na+ channels in cells obtained from CF as well as from non-CF patients showed properties different from all previously described epithelial Na+ channels (ENaC). DPC, a potent Cl- channel blocker, which has never been described to block ENaC, inhibited a considerable portion of the amiloride-sensitive Na+ absorption. In contrast to classical ENaC, cAMP induced no activation of amiloride-sensitive short-circuit current. Aldosterone failed to induce any functional stimulation of Na+ absorption in vitro when applied to the cell culture medium prior to measurements. Together with the reportedly reversible inhibition by phenamil we propose that Na+ absorption in human nasal epithelia is either regulated differently or is mediated by a yet still unknown member of the ENaC superfamily.
我们在改良的尤斯灌流小室中，对源自人鼻囊性纤维化（CF）和非CF上皮的原代培养上皮细胞融合单层中的Na⁺吸收进行了表征。来自CF患者以及非CF患者的细胞中的氨氯地平敏感Na⁺通道显示出与所有先前描述的上皮Na⁺通道（ENaC）不同的特性。DPC是一种有效的Cl⁻通道阻滞剂，从未被描述为可阻断ENaC，但它却抑制了相当一部分氨氯地平敏感的Na⁺吸收。与经典的ENaC不同，cAMP并未诱导氨氯地平敏感短路电流的激活。在测量前将醛固酮应用于细胞培养基时，它未能在体外诱导对Na⁺吸收的任何功能刺激。结合据报道苯那明的可逆抑制作用，我们提出人鼻上皮中的Na⁺吸收要么受到不同的调节，要么由ENaC超家族中一个仍未知的成员介导。
