DiBona D R, Sherman B, Bobrycki V A, Mills J W, Macknight A D
J Membr Biol. 1981 May 15;60(1):35-44. doi: 10.1007/BF01870830.
The natriferic action of vasopressin has been investigated with morphological studies of voltage-clamped toad urinary bladders. Granular cell swelling can be induced in the presence of isoosmotic solutions when the orientation of the transmural potential is reversed by voltage clamping (V.A. Bobrycki, J. W. Mills, A.D.C. Macknight & D. R. DiBona, J. Membrane Biol., 60:21, 1981) and results from an increased rate of sodium entry across the mucosal membrane; under these conditions the active transport mechanism at the basal-lateral membrane becomes rate-limiting. Vasopressin exacerbated the voltage-reversal-induced swelling of granular cells while other cell types were unaffected. Granular cell swelling appeared to be dependent upon sodium entry from the mucosal medium since it was completely prevented by amiloride. There was no evidence for an effect of vasopressin on tight junction permeability; voltage-reversal induced the same amount of junction blistering whether or not vasopressin was present. It is concluded that the predominant effect of vasopressin on transepithelial sodium transport is to increase the sodium conductance of the mucosal plasma membrane. As is the case with the hydroosmotic effect of the hormone, the natriferic action of vasopressin seems to be exerted primarily, if not entirely, on the granular cells.
利用电压钳制蟾蜍膀胱的形态学研究,对血管加压素的促钠作用进行了研究。当通过电压钳制使跨膜电位的方向反转时,在等渗溶液存在的情况下可诱导颗粒细胞肿胀(V.A. 博布里茨基、J.W. 米尔斯、A.D.C. 麦克奈特和D.R. 迪博纳,《膜生物学杂志》,60:21,1981),这是由于跨黏膜膜的钠进入速率增加所致;在这些条件下,基底外侧膜的主动转运机制成为限速因素。血管加压素加剧了电压反转诱导的颗粒细胞肿胀,而其他细胞类型未受影响。颗粒细胞肿胀似乎依赖于从黏膜介质中进入的钠,因为氨氯吡咪可完全阻止这种肿胀。没有证据表明血管加压素对紧密连接通透性有影响;无论是否存在血管加压素,电压反转诱导的连接泡数量相同。结论是,血管加压素对跨上皮钠转运的主要作用是增加黏膜质膜的钠电导。与该激素的水渗透作用一样,血管加压素的促钠作用似乎主要(如果不是完全)作用于颗粒细胞。