Micropuncture determination of pH, PCO2, and total CO2 concentration in accessible structures of the rat renal cortex.

DuBose, Thomas D.; Pucacco, Leo R.; Lucci, M. S.; Carter, Norman W.

doi:10.1172/jci109485

Cited by 76 publications

(46 citation statements)

References 26 publications

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“…Moreover, a reduction in RBF is only one possible explanation for the higher Pco2 values. Recent work has implicated chemical disequilibrium between C02 and HCO3 in the renal vasculature and vascularvascular exchange of C02 as factors contributing to the high Pco2 in the renal cortex (16,17). Whether these factors contribute to the differences in cortical Pco2 between control and CMA rats remains a subject for future investigation.…”

Section: Discussionmentioning

confidence: 99%

“…The loops were confirmed as being the last accessible proximal convolutions by the failure of a small injected oil droplet to reappear in any subsequent proximal loop on the surface of the kidney. Timed collections (5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20) Pco2 measurements. The Pco2 microelectrodes used in these studies were constructed as described previously (8), and had outer tip diameters of [4][5][6][7][8][9][10] The ability of our microelectrode system to detect small differences in Pco2, with the recorder set at 1 mV = 5 mm, was tested by using it to measure Pco2 in three solutions equilibrated with known gas mixtures (Pco2 values of 30.9, 32.4, and 35.9 mmHg as determined by Scholander analysis).…”

Section: Methodsmentioning

confidence: 99%

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Proximal tubular bicarbonate reabsorption and PCO2 in chronic metabolic alkalosis in the rat.

Maddox¹,

Gennari²

1983

J. Clin. Invest.

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A B S T R A C T Studies were undertaken to define the pattern of proximal tubular bicarbonate reabsorption and its relation to tubular and capillary Pco2 in rats with chronic metabolic alkalosis (CMA). CMA was induced by administering furosemide to rats ingesting a low electrolyte diet supplemented with NaHCO3 and KHC03. Proximal tubular bicarbonate reabsorption and Pco2 were measured in CMA rats either 4-7 or 11-14 d after furosemide injection, in order to study a wide range of filtered bicarbonate loads. A group of nine age-matched control animals, fed the same diet but not given furosemide, was studied for comparison. In a third group of controls, the filtered load of bicarbonate was varied over the same range as in the CMA rats by plasma infusion and aortic constriction. The CMA rats had significant alkalemia and hypokalemia (4-7 d: pH 7.58, HCO3 38.3 meq/liter, K+ 2.1 meq/liter; 11-14 d: pH 7.54, HCO3 38.1 meq/liter, K+ 2.5 meq/liter). Nonetheless, proximal bicarbonate reabsorption was not significantly different from that seen in control rats at any given load of filtered bicarbonate (from 250 to 1,300 pmol/min). In both control and CMA rats, 83-85% of the filtered bicarbonate was reabsorbed by the end of the accessible proximal tubule. These observations indicate that proximal bicarbonate reabsorption is determined primarily by the filtered load in chronic metabolic alkalosis. When single nephron glomerular filtration rate (SNGFR) is reduced by volume depletion in the early postfurosemide period, the filtered load and the rate of proximal bicarbonate reabsorption remain at or below control lev-

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Proximal tubular bicarbonate reabsorption and PCO2 in chronic metabolic alkalosis in the rat.

Maddox¹,

Gennari²

1983

J. Clin. Invest.

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“…30 The luminal pH is highly acidic in the medullary ray and at the outer stripe of the outer medulla, where the straight portion of the proximal tubule (S3) is located. [35][36][37][38][39] Importantly, a detailed histologic analysis revealed that 8-OHdG-ir cells were concomitantly distributed around the medullary ray and at the outer stripe of the outer medulla. Consistent with this observation, the histochemical analysis using LTL as well as the flow cytometric analysis using an anti-CD13 antibody demonstrated that albuminuria-induced oxidative stress was prominent in proximal tubular cells.…”

Section: Effect Of Luminal Alkalinization On Protein-overload Nephropmentioning

confidence: 99%

“…35,36 Furthermore, another report showed that the pH of the distal portion of proximal tubule was even lower, i.e., pH 6.2, in acidotic rats. 37 However, the pH level that was directly determined in those studies was measured only at accessible superficial sites (S1 and S2).…”

mentioning

confidence: 99%

Luminal Alkalinization Attenuates Proteinuria-Induced Oxidative Damage in Proximal Tubular Cells

Souma¹,

Abe²,

Moriguchi³

et al. 2011

Journal of the American Society of Nephrology

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alkalinization abrogates proteinuria-induced tubular damage, we studied a mouse model of protein-overload nephropathy. NaHCO 3 feeding selectively alkalinized the urine and dramatically attenuated the accumulation of O 2 ⅐ Ϫ -induced DNA damage and proximal tubular injury. Overall, these observations suggest that luminal acidity aggravates proteinuria-induced tubular damage and that modulation of this acidic environment may hold potential as a therapeutic target for proteinuric kidney disease.

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“…The reason for this pH dependence may reside in the fact that the protonated form of ferryl heme (Fe(IV)OH Ϫ ) is the reactive species, which is formally equivalent to a hydroxyl radical coordinated to ferric heme. It is important to note that renal tubular fluid is relatively acidic and the pH of the surrounding interstitium decreases further during low blood flow states (41). Thus, MetMb deposited in the renal tubules is in a milieu that greatly promotes the ability of Mb to induce lipid peroxidation.…”

Section: Effect Of Alkalinization On the Stability Of Ferryl-mb And Cmentioning

confidence: 99%

A Causative Role for Redox Cycling of Myoglobin and Its Inhibition by Alkalinization in the Pathogenesis and Treatment of Rhabdomyolysis-induced Renal Failure

Moore¹,

Holt²,

Patel³

et al. 1998

Journal of Biological Chemistry

249

222

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Muscle injury (rhabdomyolysis) and subsequent deposition of myoglobin in the kidney causes renal vasoconstriction and renal failure. We tested the hypothesis that myoglobin induces oxidant injury to the kidney and the formation of F 2 -isoprostanes, potent renal vasoconstrictors formed during lipid peroxidation. In low density lipoprotein (LDL), myoglobin induced a 30-fold increase in the formation of F 2 -isoprostanes by a mechanism involving redox cycling between ferric and ferryl forms of myoglobin. In an animal model of rhabdomyolysis, urinary excretion of F 2 -isoprostanes increased by 7.3-fold compared with controls. Administration of alkali, a treatment for rhabdomyolysis, improved renal function and significantly reduced the urinary excretion of F 2 -isoprostanes by ϳ80%. EPR and UV spectroscopy demonstrated that myoglobin was deposited in the kidneys as the redox competent ferric myoglobin and that it's concentration was not decreased by alkalinization. Kinetic studies demonstrated that the reactivity of ferryl myoglobin, which is responsible for inducing lipid peroxidation, is markedly attenuated at alkaline pH. This was further supported by demonstrating that myoglobin-induced oxidation of LDL was inhibited at alkaline pH. These data strongly support a causative role for oxidative injury in the renal failure of rhabdomyolysis and suggest that the protective effect of alkalinization may be attributed to inhibition of myoglobin-induced lipid peroxidation.

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Micropuncture determination of pH, PCO2, and total CO2 concentration in accessible structures of the rat renal cortex.

Cited by 76 publications

References 26 publications

Proximal tubular bicarbonate reabsorption and PCO2 in chronic metabolic alkalosis in the rat.

Proximal tubular bicarbonate reabsorption and PCO2 in chronic metabolic alkalosis in the rat.

Luminal Alkalinization Attenuates Proteinuria-Induced Oxidative Damage in Proximal Tubular Cells

A Causative Role for Redox Cycling of Myoglobin and Its Inhibition by Alkalinization in the Pathogenesis and Treatment of Rhabdomyolysis-induced Renal Failure

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