Effect of barium on potassium transport in amphibian kidney

We have examined the effect of barium on K excretion and transport in the perfused frog kidney. The transepithelial secretory flux of K was calculated from the rate of excretion of 42K from the portal circulation. Barium was applied to the basolateral surfaces of the tubules via the portal circulation. Barium (0.1 mM) increased fractional K excretion from 55 to 178% by stimulating the K secretory flux; 0.5 mM Ba increased fractional K excretion from 39 to 386% primarily by increasing the secretory flux greater than 10-fold. Tissue content increased 10%. When Ba was applied to both the apical and basolateral surfaces by perfusion of the arterial circulation, K excretion and secretion also increased. This same result was obtained when K secretion was first stimulated by acetazolamide. In another series of experiments, tubular cells were loaded with 42K via a pulse injection into the portal circulation, and simultaneous washout of the isotope into the urine and the venous effluent was measured. Analysis of the washout curves revealed that basolateral (portal) application of Ba inhibited efflux of K from the cells into the circulation, reduced the influx from the circulation, and stimulated efflux into the urine. We suggest that blockade of K channels in the basolateral membrane indirectly depolarizes the apical membrane and thereby increases the electrochemical gradient favoring K movement from cells to tubular fluid. When Ba is applied simultaneously to both tubular surfaces, the effect on the basolateral surface apparently overrides any direct effect it may have on K movement across the apical surface. Using 133Ba, we measured a very small transepithelial perfusate-to-tubular fluid flux. However, fractional Ba reabsorption averaged 19% when 0.5 mM Ba was present in the arterial perfusate.