Increased of heparanase expression in hypoxic/INS; endothelial cells and kidney ischemic-reperfusion injury associates with endothelin-1 elevation and eNOS reduction

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excretion, inner medullary (IM) ET receptor (ETR) expression from mice on a NSD or 7 day high salt diet (7DHS) and the response of ET1 mediated epithelial sodium channel (ENaC) activity in flox and CDNOS1KO mice. ET-1 excretion was similar between NSD flox and CDNOS1KO mice (0.14 ± 0.02 and 0.17 ± 0.06 pg/day, n = 10) and significantly increased similarly after a 7DHS (0.60 ± 0.1 and 0.60 ± 0.08 pg/day). IM ETR expression was similar between the mice on a NSD (~40% ETA, ~60% ETB receptors) and similarly shifted to ~95% ETB expression on a 7DHS. Basal CD ENaC open probability (Po) was similar (flox: 0.3 ± 0.08 CDNOS1KO: 0.3 ± 0.05). Acute ET1 treatment significantly reduced ENaC Po from flox mice but not CDNOS1KO mice compared to basal (flox 0.1 ± 0.03 and CDNOS1KO 0.3 ± 0.05, n = 6 animals P b 0.05). In conclusion, CD NOS1 appears not to regulate renal ET-1 production or ETR expression. However, the mechanism of ET-1 inhibition of CD ENaC is via NOS1. We propose that the salt-dependent increase in BP and Na retention observed in CDNOS1KO mice is mediated by the loss of ET signaling in the CD.

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