Isolated renal cortical collecting tubules from rabbits were studied at random (control) and from rabbits maintained on diets containing either high or low Na and K content or injected with DOCA for up to 31 days. In general, the values of transepithelial voltage (VT) and electrical resistance (RT) varied considerably between tubules. When rabbits were fed a high K, low Na diet or were injected with DOCA the values of VT increased. Of interest was the observation that tubules obtained from rabbits maintained on DOCA for 11-18 days or longer possessed markedly elevated values of VT (mean VT, -54 mV) and a marked increase in their ability to reabsorb Na and secrete K at rates well above the levels observed even at 3-6 days of treatment when it was expected that maximal transport rates would have been achieved. From the estimates of the conductances of Na, K, and Cl, the data could be interpreted to mean that DOCA caused a decrease in the conductance of Cl, perhaps via the shunt pathway, while elevating the conductances of Na and K, thereby enhancing active Na and especially K transport by this nephron segment.

Studies were done to test the idea that the emf of the sodium pump (ENa) of isolated frog skin could be estimated directly from studies of its current-voltage relationship. ENa was estimated in two ways: a) from the bidirectional sodium flux ratio according to Ussing and Zerahn, and b) from the values of open-circuit voltage, short-circuit current, and the shunt resistance estimated when the [Na] of the outer solution was reduced to zero. When the values of ENa were compared with the values of E1 obtained from the current-voltage relationships, they were found to be the same despite considerable variability in the values of ENa between skins (77-168 mV). In general, the values of ENa were considerably higher when the skins were bathed with sulfate-Ringer as compared with chloride-Ringer solution. These data are compatible with the idea that in nonedge-damaged frog skin, the unidirectional sodium fluxes were confined primarily to active transport pathways alone, and, accordingly, they may be excluded from parallel-shunt pathways.

Studies were done to determine the influence of vasopressin and amiloride on the sodium backflux of nonedge-damaged frog skin. As before, the bidirectional fluxes of sodium appeared to be limited primarily to the active transport pathways of control skins. When the skins were treated with vasopressin, the sodium backflux was increased selectively (over that of sucrose) and more so than was expected for the active transportpathway alone. In control skins, amiloride had no effect on the flux of the shunt pathway. However, with vasopressin-treated skins, amiloride at 10(-6) M decreased the sodium backflux of the shunt pathway to levels observed previously for the control skins. These observations are compatible with the idea that the shunt pathway may in part be cellular and in part extracellular. When the changes in open-circuit voltage and shunt resistance caused by vasopressin and amiloride (as determined from the I-V relationships) were examined, the data were also found to be compatible with the idea that vasopressin exerted an influence on the shunt pathway of the frog skin, and this effect of vasopressin could be reversed by amiloride.

No abstract