Blazer-Yost B L, Cox M
Department of Medicine, Veterans Administration Medical Center, Philadelphia, Pennsylvania.
Am J Physiol. 1988 Sep;255(3 Pt 1):C413-7. doi: 10.1152/ajpcell.1988.255.3.C413.
Insulin-like growth factor 1 (IGF1) stimulates vectorial Na+ transport in a classical model of the mammalian distal nephron, the toad urinary bladder. Net mucosal to serosal Na+ flux is stimulated by concentrations of IGF1 as low as 0.1 nM, and the response is maximal at 10 nM. Na+ transport increases within minutes of the serosal addition of IGF1, reaches a maximum in 2-3 h, and is sustained for at least 5 h. Neither the initial nor the sustained response to IGF1 is dependent on a new protein synthesis. The IGF1 response is inhibited by a concentration of amiloride (10(-5) M) that is known to specifically block the conductive apical Na+ channel but that has little effect on the Na+-H+ antiporter. Further studies will be necessary to establish a role for this growth factor in normal renal epithelial function, but it is possible that the natriferic and growth-stimulatory effects of IGF1 are intimately related.
胰岛素样生长因子1（IGF1）在哺乳动物远端肾单位的经典模型——蟾蜍膀胱中刺激向量性Na⁺转运。低至0.1 nM的IGF1浓度即可刺激从黏膜到浆膜的净Na⁺通量，且在10 nM时反应最大。在浆膜添加IGF1后几分钟内，Na⁺转运增加，在2 - 3小时内达到最大值，并持续至少5小时。对IGF1的初始反应和持续反应均不依赖于新的蛋白质合成。IGF1反应受到已知能特异性阻断顶端导电Na⁺通道但对Na⁺-H⁺反向转运体影响很小的氨氯地平浓度（10⁻⁵ M）的抑制。有必要进行进一步研究以确定这种生长因子在正常肾上皮功能中的作用，但IGF1的促钠排泄和生长刺激作用可能密切相关。
