Active transepithelial potassium transport in frog skin via specific potassium channels in the apical membrane.

In frog skin bathed in Cl--Ringer's solution the short circuit current (SCC) is equal to the net Na+ flux. In the present study Na+ and K+ transport across frog skin have been investigated in skins bathed in a solution where all Cl- has been substituted by the impermeable anion gluconate. In this solution the net Na+ flux (9.22 +/- 0.72 nmole/cm2/min) was significantly higher than the SCC (7.61 +/- 0.63) nmole/cm2/min). Measurement of the transepithelial K+ influx and K+ efflux showed that the discrepancy between the net Na+ flux and the SCC was caused by an active outwards going transepithelial K+ transport. The K+ but not the Na+ transport could be blocked by adding the K+ channel blocking agent Ba++ to the apical solution. Thus, the K+ transport occurs via a K+ specific pathway in the apical membrane. Ouabain blocked both the Na+ and the K+ transport, whereas the presence of the Na+ channel blocking agent amiloride in the apical solution blocked the Na+ transport and reduced the K+ transport. In the presence of amiloride in the apical solution the SCC and the transepithelial potential difference (PD) reversed so that the outside (the apical side) of the frog skin became positive with respect to the basolateral side. The inverted SCC was carried by an active transepithelial K+ transport, this K+ transport required the presence of Na+ in the basolateral solution. The experiments show that frog skin can insert or activate K+ channels in the apical membrane, indicating that the frog may regulate its K+ content by varying the K+ permeability of the apical membrane.