Inhibition of apical Na+ channels in rabbit cortical collecting tubules by basolateral prostaglandin E2 is modulated by protein kinase C.
作者： B N Ling , K E Kokko , D C Eaton
DOI: 10.1172/JCI115998
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摘要: Abstract We used the cell-attached patch clamp technique to investigate interaction of exogenous prostaglandins (PG), intracellular [Ca2+]i, and protein kinase C (PKC) on high selectivity, 4 pS Na+ channel found in principal cell apical membrane rabbit cortical collecting tubule (CCT) cultures grown collagen supports with 1.5 microM aldosterone. Application 0.5 PGE2 basolateral decreased mean NP0 (number channels times open probability) for by 46.5% (n = 9). There was no consistent change after 12) or PGF2 alpha 8). Release [Ca2+]i stores 0.25 thapsigargin 7), activation PKC 0.1 beta-phorbol-12-myristate-13-acetate 5) 10 1-oleyl-2-acetylglycerol 4) also NP0. Depletion (0.25 pretreatment) 7) inhibition (100 D-sphingosine 8) abolished inhibitory effects PGE2. Conclusions: (a) transport CCT cells is modulated PGE2; (b) mechanism involves release IP3-sensitive, stores; (c) Ca(2+)-dependent PKC, which then inhibits channels.
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