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      Altered Regulation of type 3 Na +/H + exchanger, type 1 Na +/HCO 3 - cotransporter, and Na +,K +-ATPase in the Kidney of Rats with Experimental Rhabdomyolysis

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          Abstract

          Metabolic acidosis was shown to correlate with deterioration of renal function in patients with rhabdomyolysis. The present study was aimed to investigate whether the changes of type 3 Na +/H + exchanger (NHE3), type 1 Na +/HCO 3 - cotransporter (NBC1), and Na +,K +-ATPase α1 subunit may play a role in the pathogenesis of metabolic acidosis in glycerol-induced experimental rhabdomyolysis. Male Sprague-Dawley rats were deprived of fluid intake for 24 hours, and then were injected with 50% glycerol in normal saline (10 mL/kg, intramuscularly). At 24 hours after the glycerol injection, rats were sacrificed by decapitation. Control rats were injected with normal saline. The protein expression of NHE3, NBC1 and Na +,K +-ATPase α1 subunit was determined in the cortex of the kidney by immunoblotting and immunohistochemistry. Following the treatment of glycerol, creatinine clearance was significantly decreased, and high anion gap metabolic acidosis developed. In the experimental group, the expression of Na +,K +-ATPase α1 subunit was significantly decreased in the cortex of the kidney. On the contrary, the expression of NHE3 and NBC1 was significantly increased. Immunohistochemical analyses confirmed the immunoblotting data. In conclusion, the coordinate up-regulation of NHE3 and NBC1 may play an adaptive role against the metabolic acidosis in glycerol-induced rhabdomyolysis.

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          Rhabdomyolysis.

          R Vanholder, E Erek, N Lameire … (2000)
          Article 0 comments Cited 110 times – based on 0 reviews     Review now
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            Intracellular pH regulation in the renal proximal tubule of the salamander. Basolateral HCO3- transport

            WF Boron, E. Boulpaep, W. F. Boron (1983)
            We have used pH-, Na-, and Cl-sensitive microelectrodes to study basolateral HCO3- transport in isolated, perfused proximal tubules of the tiger salamander Ambystoma tigrinum. In one series of experiments, we lowered basolateral pH (pHb) from 7.5 to 6.8 by reducing [HCO3-]b from 10 to 2 mM at a constant pCO2. This reduction of pHb and [HCO3-]b causes a large (approximately 0.35), rapid fall in pHi as well as a transient depolarization of the basolateral membrane. Returning pHb and [HCO3-]b to normal has the opposite effects. Similar reductions of luminal pH (pHl) and [HCO3-]l have only minor effects. The reduction of [HCO3-]b and pHb also produces a reversible fall in aiNa. In a second series of experiments, we reduced [Na+]b at constant [HCO3-]b and pHb, and also observed a rapid fall in pHi and a transient basolateral depolarization. These changes are reversed by returning [Na+]b to normal. The effects of altering [Na+]l in the presence of HCO3-, or of altering [Na+]b in the nominal absence of HCO3-, are substantially less. Although the effects on pHi and basolateral membrane potential of altering either [HCO3-]b or [Na+]b are largely blocked by 4-acetamido-4- isothiocyanostilbene-2,2'-disulfonate (SITS), they are not affected by removal of Cl-, nor are there accompanying changes in aiCl consistent with a tight linkage between Cl- fluxes and those of Na+ and HCO3-. The aforementioned changes are apparently mediated by a single transport system, not involving Cl-. We conclude that HCO3- transport is restricted to the basolateral membrane, and that HCO3- fluxes are linked to those of Na+. The data are compatible with an electrogenic Na/HCO3 transporter that carries Na+, HCO3-, and net negative charge in the same direction.
            Article 0 comments Cited 31 times – based on 0 reviews     Review now
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              Hemoglobin- and myoglobin-induced acute renal failure in rats: role of iron in nephrotoxicity.

              M Paller (1988)
              In ischemic acute renal failure oxygen free radicals may mediate injury. In addition, iron appears to play a critical role in hydroxyl radical formation and lipid peroxidation during reperfusion of ischemic kidneys. To determine whether iron may play a similar role in pigment (heme protein)-induced acute renal failure, we studied the effects of the iron chelator deferoxamine in two experimental models of pigment-induced acute renal failure, intramuscular glycerol injection and intravenous hemoglobin infusion without and with concurrent ischemia in the rat. Intramuscular injection of 50% glycerol (5 ml/kg) caused inulin clearance to fall to 0.13 +/- 0.03 (SE) ml/min (normal value, 1.0-1.2 ml/min). Continuous infusion of deferoxamine beginning at the time of glycerol injection significantly attenuated this renal dysfunction. Deferoxamine-treated animals had an inulin clearance of 0.37 +/- 0.06 ml/min (P less than 0.01). Glycerol injection was also associated with significant lipid peroxidation, measured as renal malondialdehyde content. Deferoxamine-treated glycerol-injected rats had renal malondialdehyde content not significantly different from control animals. In another model of heme pigment-induced renal injury, hemoglobin was infused to produce hemoglobinuria. Inulin clearance 1 h after hemoglobin infusion was significantly reduced to 0.84 +/- 0.5 ml/min (P less than 0.025). Infusion of deferoxamine after hemoglobin prevented the hemoglobin-induced decrease in inulin clearance. Thirty minutes of renal ischemia followed by infusion of hemoglobin resulted in more severe renal dysfunction with inulin clearance of 0.54 +/- 0.08 ml/min. Deferoxamine infused at the time of reperfusion attenuated the fall in glomerular filtration rate after ischemia and hemoglobin infusion:inulin clearance 1.04 +/- 0.07 (P less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)
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                Author and article information

                Journal
                Journal ID (nlm-ta): Electrolyte Blood Press
                Journal ID (iso-abbrev): Electrolyte Blood Press
                Journal ID (publisher-id): EBP
                Title: Electrolytes & Blood Pressure : E & BP
                Publisher: The Korean Society of Electrolyte and Blood Pressure Research
                ISSN (Print): 1738-5997
                ISSN (Electronic): 2092-9935
                Publication date (Print): December 2007
                Publication date (Electronic): 31 December 2007
                Volume: 5
                Issue: 2
                Pages: 55-61
                Affiliations
                [1 ]Department of Internal Medicine, Chonnam National University Medical School, Gwangju, Korea.
                [2 ]Department of Physiology, Chonnam National University Medical School, Gwangju, Korea.
                [3 ]Department of Physiology, Chonbuk National University Medical School, Jeonju, Korea.
                Author notes
                Corresponding author: Soo Wan Kim, M.D. Department of Internal Medicine, Chonnam National University Medical School, 8 Hak-dong, Dong-gu, Gwangju, 501-757, Korea. Tel: +82-62-220-6272, Fax: +82-62-225-8578, skimw@ 123456chonnam.ac.kr
                Article
                DOI: 10.5049/EBP.2007.5.2.55
                PMC ID: 3894516
                SO-VID: 288d1b3a-7518-48e5-ab96-b61dd1dcec2f
                Copyright © Copyright © 2007 The Korean Society of Electrolyte and Blood Pressure Research
                History
                Date received : 01 October 2007
                Date accepted : 12 October 2007
                Categories
                Subject: Original Article

                ScienceOpen disciplines: Cardiovascular Medicine
                Keywords: rhabdomyolysis,metabolic acidosis,type 3 na+/h+ exchanger,type 1 na+/hco3- cotransporter
                Data availability:
                ScienceOpen disciplines: Cardiovascular Medicine
                Keywords: rhabdomyolysis, metabolic acidosis, type 3 na+/h+ exchanger, type 1 na+/hco3- cotransporter

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