Proceedings of the Physiological Society, 22‐23 July 1988, Cambridge Meeting: Communications

Abstract

Apical membrane sodium co-transport stimulation is associated with cell depolarization followed by partial recovery of potential over several minutes in a variety of lealky epithelia including amphibian and mammalian renal proximal tubules (Lang et al. 1986). Recent observations from this laboratory implicated the basolateral sodium bicarbonate transporter in the recovery of potential in the rabbit proximal tubule (Beck et al. 1987a). In the frog proximal tubule the recovery has been shown to be at least partly due to an increase in basolateral potassium conductance (Lang et al. 1986). We now report observations designed to examine the possibility that changes in the basolateral potassium conductance may also contribute to the recovery of cell potential in the rabbit proximal tubule.Grade IV specific pathogen free New Zealand White rabbits of either sex were anaesthetized with pentobarbitone (35 mg kg-' i.v.), the left kidney flushed with preservation fluid, removed and proximal convoluted tubule segments set up for microperfusion in vitro with measurement of VBL (Beck et al. 1986). Peritubular potassium was then briefly (< 5 s) stepped from 5 to 20 mm (in place of sodium) before, during and after stimulation of apical sodium co-transport by introduction of glucose and alanine (replacement of mannitol) into the lumen (Beck et al. 1987b). Initially, when VBL was -53-2 + 4-5 (S.E.M., n = 5) mV, potassium steps caused brief superimposed depolarizations of 86 + 25 mV. Introduction of glucose and alanine into the lumen caused the familiar transient change in PD consisting of a basolateral depolarization of 218 + 1P2 mV followed by a repolarization of 13-6 + 12 mV. At the peak of this slow depolarization, potassium steps caused depolarizations of 5-6 + 2-0 mV. However, after the slow repolarization, potassium steps caused larger depolarizations of 10-1 + 1P8 mV (P < 0 05, paired t test). When glucose and alanine were removed from the lumen the basolateral membrane hyperpolarized to -63 + 2-6 mV before return to -57 0 + 1P8 mV. Neither this final potential, nor the depolarization then elicited by potassium steps (9-8 +1 0 mV), were significantly different from control values.These results are consistent with an increase in relative basolateral potassium conductance during apical sodium cotransport stimulation in the rabbit proximal convoluted tubule.