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Evaluation of ENaC and fluid secretion along the mouse CD: Endothelin‐1 down‐regulates Na reabsorption
Author(s) -
Lynch I. Jeanette,
Cain Brian D.,
Wingo Charles S.
Publication year - 2012
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.26.1_supplement.1105.11
Subject(s) - epithelial sodium channel , reabsorption , aldosterone , endocrinology , medicine , chemistry , renal sodium reabsorption , homeostasis , kidney , angiotensin ii , renal physiology , secretion , endothelin 1 , renin–angiotensin system , distal convoluted tubule , excretion , sodium , receptor , biology , blood pressure , organic chemistry
Na homeostasis and the renin‐angiotensin‐aldosterone system are important for systemic arterial blood pressure. Aldosterone and endothelin‐1 (ET‐1) have opposing actions on Na reabsorption (J Na ) in the kidney. Aldosterone increases J Na in the collecting duct (CD) by stimulating the epithelial Na channel (ENaC). CD ET‐1 production is stimulated by aldosterone and inhibits ENaC thereby increasing Na and water excretion in part via the ET B receptor. To date, direct measurement of the quantitative effect of ET‐1 on transepithelial J Na in the native mouse CD has not been determined. These studies were performed to examine benzamil‐sensitive (1 μM) J Na in the CD and to test whether ET‐1 (20 nM) inhibits J Na . J Na was measured as 22 Na flux in isolated in vitro microperfused CD segments. We observed: 1) the CD exhibits J Na in male and female mice that is regulated, in part, by a benzamil‐sensitive pathway (presumably ENaC) and exhibits fluid secretion that is greater in females than males; and 2) ENaC‐mediated J Na is greater in the CCD than in the OMCD; however, benzamil‐insensitive J Na is present in the CCD and not in the OMCD; and 3) in the presence of ET‐1, ENaC‐mediated J Na and fluid secretion are both inhibited. We conclude: 1) Na reabsorption is mediated by ENaC in the CCD and OMCD and also by an ENaC‐independent mechanism in the CCD; and 2) ET‐1 inhibits ENaC‐mediated Na reabsorption in the CCD. Supported by NIH R01DK82680.