Prostaglandins are important in signaling pathways involved in modulating the rates of Na+ transport in a diverse group of tissues possessing apical membrane epithelial channels. PGE2 is known to cause either stimulation, inhibition or transient stimulatory changes of Na+ transport. We have continued our studies of frog skins that are known to respond to forskolin and PGE2 with large steady-state increases of transport and have used noninvasive methods of blocker-induced noise analysis of Na+ channels to determine their channel densities (N T ) and open probabilities (P o ). In the absence of exogenous hormones, baseline rates of Na+ transport are especially high in scraped skins (R. pipiens pipiens) studied in the fall of the year. Na+ transport was inhibited by indomethacin and by removal of the unstirred layers of the corium (isolated epithelia) alone suggesting that PGE2 is responsible for the sustained and elevated rates of transport in scraped skins. Changes of transport caused by indomethacin, forskolin or PGE2 were unquestionably mediated by considerably larger changes of N T than compensatory changes of P o . Since cAMP caused no change of P o in tissues pretreated with indomethacin, PGE2 appears in this tissue to serve a dual role, increasing the steady state N T by way of cAMP and decreasing P o by unknown mechanisms. Despite appreciable PGE2-related decreases of P o , the net stimulation of transport occurs by a considerably greater cAMP-mediated increase of N T .
The Journal of Membrane Biology – Springer Journals
Published: Jan 1, 1997
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