Kinetics of Na+ transport in Necturus proximal tubule.

Abstract

A B S T R A C T The dependence of proximal tubular sodium and fluid reabsorption on the Na + concentration of the luminal and peritubular fluid was studied in the perfused Necturus kidney. Fluid droplets, separated by oil from the tubular contents and identical in composition to the vascular perfusate, were introduced into proximal tubules, reaspirated, and analyzed for Na ÷ and [~4C]mannitol. In addition, fluid transport was measured in short-circuited fluid samples by observing the rate of change in length of the split droplets in the tubular lumen. Both reabsorptive fluid and calculated Na fluxes were simple, saturable functions of the perfusate Na + concentration (Kin = 35-39 mM/liter, Vmax = 1.37 control value). Intracellular Na +, determined by tissue analysis, and open-circuit transepithelial electrical potential differences were also saturable functions of extracellular Na +. In contrast, net reabsorptive fluid and Na + fluxes were linearly dependent on intracellular Na + and showed no saturation, even at sharply elevated cellular sodium concentrations. These concentrations were achieved by addition of amphotericin B to the luminal perfusate, a maneuver which increased the rate of Na + entry into the tubule cells and caused a proportionate rise in net Na + flux. It is concluded that active peritubular sodium transport in proximal tubule cells of Necturus is normally unsaturated and remains so even after amphotericin-induced enhancement of luminal Na ÷ entry. Transepithelial movement of NaCI may be described by a model with a saturable luminal entry step of Na ÷ or NaCI into the cell and a second, unsaturated active transport step of Na + across the peritubular cell boundary.

Dependence of water movement on sodium transport in kidney proximal tubule: A microperfusion study substituting lithium for sodium

“…The present results are somewhat in contradiction with those obtained on Necturus by Spring and Giebisch [32] and on the rat by Gyory [17]; these authors found that lowering the external Na concentration by up to half its control value did not statistically change the net water and sodium fluxes. On the other hand, the results of the present lithium experiments are in good agreement with previous observations made on rabbit proximal tubule [8].…”

“…Removal of all the Na from the external medium abolishes the water flux [4,15,17,32]. The same result is obtained by inhibiting basolateral Na-K-ATPase activity with ouabain or by depriving the bath of potassium [4,6].…”

“…6). In that case, the amount of Na entering the proximal tubule cells would be a function of its luminal concentration; Na would therefore be extruded on the basolateral side of the cell through the Na-K-ATPase system, in amounts proportional to its entry on the luminal side [32] and would be followed by the extrusion of an isoosmotic proportion of water.…”

“…Nevertheless, the relationship between net water fluxes and the external Na concentration is not yet clear. In previous works, the following protocols have been used to reduce external Na concentration: (i) replacement of Na on the luminal side by a nonpermeable substance such as sucrose or mannitol [25,37]; (ii) replacement of Na on both sides of the epithelium by cations like Li, K or choline [4,15,17,32], and (iii) lowering of the external Na concentration without replacement [8]. In the first two cases, the solution was iso-osmotic, whereas it was hypo-osmotic in the third.…”

Sodium/calcium exchange in mammalian ventricular muscle: a study with sodium‐sensitive micro‐electrodes.

“…The ability of the preparation to withstand multiple exposure to Na-poor solutions was greatest with tetramethylammonium chloride. The lenity of tetramethylammonium chloride as a Na substitute has also been noted by Spring & Giebisch (1977) Mechanical response. A number ofdifferences were found between the Na withdrawal contractures, responses to caffeine and twitches in guinea-pig and ferret.…”