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Angiotensin II Stimulates ENaC and suppresses the inhibitory effect of 11,12‐EET on ENaC in the cortical collecting duct (CCD)
Author(s) -
Sun Peng,
Lin Daohong,
Yue Peng,
Wang Wenhui
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.606.7
Subject(s) - epithelial sodium channel , losartan , chemistry , angiotensin ii , endocrinology , medicine , epoxygenase , amiloride , inhibitory postsynaptic potential , patch clamp , renin–angiotensin system , receptor , stimulation , arachidonic acid , biology , sodium , enzyme , blood pressure , biochemistry , organic chemistry
We used the patch‐clamp technique to study the effect of angiotensin II (Ang II) on ENaC in principal cell (PC) of the CCD. The amiloride‐sensitive Na currents in PC measured with perforated patch were 480¡A64 pA at −100 mV in rats on a high K (10%) diet. Application of 100 nM Ang II increased Na current by 260% to 1247¡A289 pA. However, treatment of the CCD with losartan abolished Ang II‐induced increase in Na current, suggesting that the stimulatory effect of Ang II on ENaC was the result of activating Ang II type I receptor (AT1R) which is expressed in the CCD. The stimulation of Ang II on ENaC was also observed by single channel recording: Ang II increased the ENaC activity defined by NPo from 0 to 0.4¡A0.08 within 5 min. We confirmed that addition of 100 nM 11,12‐EET (a major product of CYP epoxygenase‐dependent arachidonic acid metabolism) inhibited ENaC in the CCD in rats on a high K diet. However, the supression of EET on ENaC was significantly attenuated by application of Ang II which increased EC 50 value of 11,12‐EET‐induced inhibition from 50 to 100 nM. We conclude that acutely application of Ang II stimulates ENaC activity via AT1R‐dependent pathway and diminishes the inhibition of 11,12‐EET on ENaC.