Inhibition of Na Transport by prostacyclin (PGI2) in rabbit cortical collecting tubule.

The effects of prostacyclin (PGI2) on transepithelial potential difference (PD) and sodium transport were examined in rabbit cortical collecting tubules (CCT) perfused in vitro. Addition of PGI2 (10-6M) to the bathing medium, which was bubbled with 95% O2 - 5% CO2, caused a reversible decrease in PD averaging 49 +/- 9.4(SE)%. Maximal effect was evident between 5-10 min. after addition of PGI2 and PD returned spontaneously towards control values within 30 min., corresponding to the rapid degradation of PGI2. In a more alkaline bathing solution achieved by bubbling with 100% O2, in which the degradation of PGI2 is known to be delayed markedly, the decrease in PD by PGI2 was continuous and dose-dependent, with half-maximal and maximal effects achieved at 10-7M and 10-5M, respectively. Neither 10-8M PGI2 nor vehicle alone exerted significant effects on PD. 6-keto-PGF1 alpha (10-5M), believed to be the major metabolite of PGI2, had no effect on PD. Lumen-to-bath flux of Na decreased with PGI2 from 9.0 to 5.6 pEq/cm/sec (n=4, p less than 0.005), although bath-to-lumen flux did not change significantly. In summary, PGI2 caused a dose-dependent decrease in PD of rabbit CCT and inhibited Na absorption in this segment in vitro. These results suggest that PGI2 may play as important role in regulating Na transport in CCT.