Parker J C, Colclasure G C, McManus T J
Department of Medicine, University of North Carolina, Chapel Hill 27599-7035.
J Gen Physiol. 1991 Nov;98(5):869-80. doi: 10.1085/jgp.98.5.869.
Hypertonic shrinkage of dog red cells caused rapid activation of Na/H exchange and rapid deactivation of [K-Cl] cotransport. Hypotonic swelling caused delayed deactivation of Na/H exchange and delayed activation of [K-Cl] cotransport. Okadaic acid stimulated shrinkage-induced Na/H exchange and inhibited swelling-induced [K-Cl] cotransport. The data are compatible with the kinetic model of Jennings and Al-Rohil (1990. J. Gen. Physiol. 95:1021-1040) for volume regulation of [K-Cl] cotransport in rabbit red cells and suggest that in dog red cells Na/H exchange and [K-Cl] cotransport are controlled by a common regulatory system. The proposal of Jennings and Schulz (1991. J. Gen. Physiol. 96:799-817) that activation/deactivation of volume-sensitive transport involves phosphorylation/dephosphorylation of a regulatory protein is supported by these observations.
犬红细胞的高渗收缩导致钠/氢交换迅速激活以及[钾-氯]协同转运迅速失活。低渗肿胀导致钠/氢交换延迟失活以及[钾-氯]协同转运延迟激活。冈田酸刺激收缩诱导的钠/氢交换并抑制肿胀诱导的[钾-氯]协同转运。这些数据与詹宁斯和阿尔-罗希尔(1990年。《普通生理学杂志》95:1021-1040)关于兔红细胞[钾-氯]协同转运转运调节的动力学模型相符,并表明在犬红细胞中钠/氢交换和[钾-氯]协同转运受一个共同调节系统控制。詹宁斯和舒尔茨(1991年。《普通生理学杂志》96:799-817)提出的容积敏感转运的激活/失活涉及调节蛋白的磷酸化/去磷酸化这一观点得到了这些观察结果的支持。