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Impaired sodium excretion following recovery from ischemic acute renal failure
Author(s) -
Spurgeon Kimberly R.,
Mattson David L.,
Basile David P.
Publication year - 2006
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.20.4.a341-b
Subject(s) - fractional excretion of sodium , endocrinology , medicine , aldosterone , excretion , natriuresis , chemistry , renal function , creatinine , vasopressin , sodium , renal blood flow , renal ischemia , perfusion , kidney , ischemia , reperfusion injury , organic chemistry
This study determined alterations of pressure natriuresis (p‐n) in rats following recovery from ischemia reperfusion (I/R) induced acute renal failure (ARF). Male Sprague‐Dawley rats on 0.4% NaCl chow were subjected 40 min bilateral I/R (n=14) or control sham surgery (n=11). I/R animals transiently decreased renal function as indicated by serum creatinine (3.0 ± 0.4 mg/dl) at 24 hrs post‐surgery that returned back toward sham‐operated control values, 0.6 ± 0.3 mg/dl at 7 days post‐I/R. For determination of acute p‐n, the kidney was denervated and aldosterone, vasopressin, norepinephrine, and corticosterone were clamped by infusion. Urine flow increased from 5.4 ± 1.9 to 23 ± 2.6 μEq/min/100g bwt in sham‐operated rats as renal perfusion pressure (RPP) was increased from 107 ± 2 to 141 ± 5 mmHg. In contrast urine flow in post‐I/R rats was depressed by 19 – 34% at all levels of RPP. Sodium excretion increased from 1.2 ± 0.4 to 5.2 ± 0.6 μEq/min/100g bwt as RPP was increased. In contrast, sodium excretion in post‐I/R rats was depressed by 27 – 58% at each RPP. Fractional sodium excretion increased approximately six‐fold as RPP increased in sham‐operated controls, while post‐I/R rats did not manifest an increase. RBF and GFR remained constant over all RPP in both groups; however, the baseline RBF (2.5 ± 0.1 vs 2.1 ± 0.1 ml/min/100g bwt) and GFR (0.54 ± 0.05 vs 0.30 ± 0.30 ml/min/100g bwt) were less in post‐I/R rats. These data suggest impairment in the ability of the post‐ischemic kidney to regulate sodium excretion. Support by NIH DK‐63114 HL‐29587