Effect of high hydrostatic pressure on sodium transport across toad skin.

The short-circuit current (Isc) was measured as an index of active net sodium transport across the isolated toad skin under various hydrostatic pressures up to 300 ATA. Upon compression, the base-line Isc increased transiently during the first 10 min by 10-15 microA/cm2 (congruent to 20%) and then decreased continuously, leveling off at 40 min under pressure. The latter decrease in base-line Isc (P less than 0.05 at all pressures) was pressure dependent, and its magnitude was 30 microA/cm2 (60% inhibition) at 300 ATA. Similarly, the transepithelial electric potential difference (PD) tended to increase slightly during the early phase of compression and decreased during the steady-state phase of compression. The transepithelial resistance (R), calculated from PD/Isc ratios, generally increased under pressure. The addition of vasotocin to the inside bathing medium resulted in an increase in Isc and PD and a reduction in R at all pressures. The magnitude of peak Isc response to vasotocin was 50-60 microA/cm2 at pressures up to 100 ATA, but decreased to 30 microA/cm2 at 200-300 ATA (0.05 less than P less than 0.10 as compared to the response at 1 ATA). On the other hand the stimulatory effect of 1 mM cyclic adenosine monophosphate (cAMP), added to the inside bathing medium, on Isc was not affected by pressure between 1 and 300 ATA. From these results it is postulated that the inhibition of base-line Na transport under high hydrostatic pressure may be primarily due to a decrease in the outer membrane permeability to Na rather than an inhibition of the Na-K-ATPase.