Efflux of potassium ( 86Rb +) attenuates the volume-restorative effect of sodium-amino acid cotransport in rat renal inner medullary cells shrunken by exposure to hyperosmotic media

Abstract

When the osmolality of the bathing medium was increased from 710 to 2000 mosmol/kg H 2O, cells in incubated slices of rat renal inner medulla lost water and K +, and the rate of efflux of preloaded 86Rb + (a tracer for K +) was significantly depressed. Addition of 2-aminoisobutyric acid (AIB, 10 mmol/l) partly restored cell water content but without re-accumulation of K +; the rate of 86Rb + efflux was greatly increased. The presence of Ba 2+ (1 mmol/l) or trifluoperazine (50 μmol/l) led to complete recovery of cell volume and K + contents, with markedly reduced efflux of 86Rb +. Neither additive had any significant effect upon these variables in the absence of AIB or in media of 710 mosmol/kg. Efflux of 86Rb + was pH-sensitive within the physiological range, and was depressed when external AIB was reduced below approx. 5 mmol/l. When external Na + was increased from 145 to 500 mmol/l (total osmolality 350 to 2500 mosmol/kg) efflux was retarded only slightly if AIB was present, but markedly if AIB was omitted. Inner medullary cells may contain a class of Ba 2+-inhibitable, calmodulin-dependent K + conductive pathway which is activated in strongly hyperosmotic media by the operation of an inwardly-directed Na +-amino acid symport (cf. Law, R.O. (1988) Pflügers Arch. 413, 43–50) and which serves to moderate the volume-restorative effect of this membrane mechanism.