, Volume 396, Issue 4, pp 325-334

Properties of the basolateral membrane of the cortical thick ascending limb of Henle's loop of rabbit kidney

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Abstract

The present study utilizes the transepithelial and transmembrane electrophysiological approach to study the properties of the basolateral membrane of the in vitro perfused cortical thick ascending limb of Henle's loop (cTAL) of rabbit kidney. Eight different series were performed in a total of 119 tubules. The key observations are: 1. A K+ concentration upward step in the bath from 3.6 to 18.6 mmol · l−1 depolarizes the basolateral membrane by 19±2 mV. 2. This depolarization can be abolished when Ba2+ (3 mmol · l−1) is added to the bath: The depolarization by Ba2+ alone is equal to that by Ba2+ plus the K+ concentration upward step (21.7 versus 22.4 mV). 3. This effect of Ba2+ is not accompanied by any change in transepithelial resistance nor in the fractional resistance of the basolateral membrane. 4. A Cl concentration downward step in the bath from 150 to 50 mmol · l−1 leads to a depolarization between 8–15 mV.

We conclude that the K+ exit at the basolateral membrans is mainly electroneutral and that Cl leaves the cell both electroneutrally (KCl) and diffusionally. The present data, together with previous findings from our laboratory, are used to draw a tentative model for the NaCl reabsorption in the cTAL segment. In this model the (Na++K+)-ATPase provides the primary driving force. Na+, 2 Cl, K+ are cotransported luminally, K+ recycles across the lumen membrane. Cl leaves the cell in part in conjunction with K+, and thus utilizing the chemical gradient for K+, and the remainder leaves the cell through the Cl conductive pathway. The discrepancy of the conductivity properties of both cell membranes, the lumen membrane K+ conductive, and the basolateral membrane Cl conductive, is the main source for the lumen positive transepithelialPD. ThePD, in turn, drives a seizable fraction of the Na+ through the paracellular shunt pathway.

This study was supported by: Deutsche Forschungsgemeinschaft, Gr. 480/5-7. Parts of this study have been presented at: Int. Symp. Ototoxicity, Reinhardshausen, April 1981, 56th Meeting Deutsche Physiologische Gesellschaft 1982, 66th Meeting Federation American Society Experimental Biology 1982