Quamme G, Biber J, Murer H
Department of Medicine, University of British Columbia, Vancouver, Canada.
Am J Physiol. 1989 Dec;257(6 Pt 2):F967-73. doi: 10.1152/ajprenal.1989.257.6.F967.
Sodium-phosphate (Na-Pi) cotransport is principally regulated by parathyroid hormone (PTH) and by the intrinsic ability to "adapt" to ambient phosphate concentration. In the present study, these two control mechanisms were examined in a cloned opossum kidney (OK) cell line. PTH inhibited Na-Pi cotransport, half-maximal inhibition at 5 x 10(-12) M, by fractionally similar amounts irrespective of the initial transport rates predetermined by "adaptation" to media phosphate concentration. At maximal concentrations of PTH (10(-8) M), the residual Na-Pi cotransport activity was higher in cells exposed to low-phosphate media. Cells preexposed to PTH (10(-8) M) or dibutyryl adenosine 3'-5'-cyclic monophosphate (DBcAMP) (10(-5) M) and forskolin (10(-5) M) increase transport (adaptation) by fractionally similar amounts as control cells for any given external phosphate concentration. The protein kinase C inhibitor, staurosporine, prevented PTH action but did not alter the ability to adapt Na-Pi cotransport in response to low media phosphate concentration. These data support the notion that regulation of Na-Pi cotransport by PTH and the adaptive response to available media phosphate concentration are distinct regulatory control mechanisms.
钠-磷酸盐（Na-Pi）共转运主要受甲状旁腺激素（PTH）以及“适应”环境磷酸盐浓度的内在能力调节。在本研究中，在克隆的负鼠肾（OK）细胞系中研究了这两种控制机制。PTH抑制Na-Pi共转运，在5×10⁻¹² M时半数最大抑制，无论通过“适应”培养基磷酸盐浓度预先确定的初始转运速率如何，抑制程度相似。在PTH的最大浓度（10⁻⁸ M）下，暴露于低磷酸盐培养基的细胞中残余的Na-Pi共转运活性更高。预先暴露于PTH（10⁻⁸ M）或二丁酰腺苷3'-5'-环磷酸单酯（DBcAMP）（10⁻⁵ M）和福斯可林（10⁻⁵ M）的细胞，对于任何给定的外部磷酸盐浓度，其转运增加（适应）的程度与对照细胞相似。蛋白激酶C抑制剂星形孢菌素可阻止PTH的作用，但不会改变Na-Pi共转运对低培养基磷酸盐浓度作出反应的适应能力。这些数据支持这样的观点，即PTH对Na-Pi共转运的调节以及对可用培养基磷酸盐浓度的适应性反应是不同的调节控制机制。
