Vasotocin has the potential to inhibit basolateral Na(+)/K (+)-pump current across isolated skin of tree frog in vitro, via its V(2)-type receptor/cAMP pathway.

Adult frog skin transports Na(+) from the apical to the basolateral side across the skin. Antidiuretic hormone (ADH) is involved in the regulation of Na(+) transport in both mammals and amphibians. We investigated the effect of arginine vasotocin (AVT), the ADH of amphibians, on the short-circuit current (SCC) across intact skin and on the basolateral Na(+)/K(+)-pump current across apically nystatin-permeabilized skin of the tree frog, Hyla japonica, in which the V(2)-type ADH receptor is expressed in vitro. In intact skin, 1 pM AVT had no effect on the SCC, but 10 nM AVT was sufficient to stimulate the SCC since 10 nM and 1 microM of AVT increased the SCC 3.2- and 3.4-fold, respectively (P > 0.9). However, in permeabilized skin, AVT (1 microM) decreased the Na(+)/K(+)-pump current to 0.79 times vehicle control. Similarly, 500 microM of 8Br-cAMP increased the SCC 3.2-fold, yet 1 mM of 8Br-cAMP decreased the Na(+)/K(+)-pump current to 0.76 times vehicle control. Arachidonic acid (10(-5) M) tended to decrease the Na(+)/K(+)-pump current. To judge from these in vitro experiments, AVT has the potential to inhibit the basolateral Na(+)/K(+)-pump current via the V(2)-type receptor/cAMP pathway in the skin of the tree frog.