Determination of disequilibrium pH in the rat kidney in vivo: evidence of hydrogen secretion

DuBose, Thomas D.; Pucacco, Leo R.; Carter, N. W.

doi:10.1152/ajprenal.1981.240.2.f138

Cited by 33 publications

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“…Thus, although small in magnitude, hydrogen secretion must occur in the distal tubule during control conditions and after the induction of a chronic acidosis. These findings contrast with those of Lucci et al (18) and DuBose et al (32), who used bicarbonate reabsorption as an index of hydrogen ion secretion. The present studies suggest that ammonia rather than bicarbonate is the major proton acceptor in the distal segment of surface nephrons.…”

Section: Discussioncontrasting

confidence: 91%

Contribution of individual superficial nephron segments to ammonium handling in chronic metabolic acidosis in the rat. Evidence for ammonia disequilibrium in the renal cortex.

Simon¹,

Martin²,

Buerkert³

1985

J. Clin. Invest.

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Ammonia entry along surface nephron segments of rats was studied with micropuncture techniques under control and chronic metabolic acidosis conditions. Tubule fluid was collected successively from sites at the end and beginning of the distal tubule and at the end of the proximal tubule of the same nephron. During chronic metabolic acidosis, ammonium excretion doubled. As anticipated, the ammonium concentration (TFNHO3 was significantly higher in proximal tubule fluid during acidosis, and ammonium delivery to end proximal sites increased from 19.4±2.3 to 34.0±3.2 pmol/min (P < 0.001). Although chronic acidosis did not affect TFNW at the beginning of the distal tubule, ammonium delivery to the end of the distal tubule increased from 5.72±0.97 to 9.88±0.97 pmol/min. In both control and acidotic groups ammonium delivery was lower (P < 0.001) to end distal sites than to end proximal sites, indicating net loss in the intervening segment. This loss was greater during chronic metabolic acidosis (23.9±33 vs. 13.6±2.0 pmol/min in controls, P < 0.025). In both groups net entry of ammonia, in similar amounts, occurred along the distal tubule (P < 0.05). In situ pH averaged 6.80±0.05 at end proximal tubule sites and fell to 6.54±0.08 at the beginning of the distal tubule (P < 0.005). Chronic metabolic acidosis did not affect these measurements. The calculated free ammonia at the end of the proximal tubule rose from 93±2.2 to 21±9 iM (P < 0.005) during chronic metabolic acidosis, and was also higher at beginning distal sites during acidosis (8.8±2.4 vs.2.7±0.7 uM in controls, P < 0.05). In both groups ammonia values for the beginning distal tubule fluid were lower than for end proximal tubule fluid. Thus, loss of ammonium in the loop segment is enhanced by chronic metabolic acidosis. Distal entry of ammonia is markedly less than along the proximal tubule and does not change in chronic metabolic acidosis, and ammonia permeabilities for the proximal and distal segments of surface nephrons seem different.

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Section: Discussioncontrasting

confidence: 91%

Contribution of individual superficial nephron segments to ammonium handling in chronic metabolic acidosis in the rat. Evidence for ammonia disequilibrium in the renal cortex.

Simon¹,

Martin²,

Buerkert³

1985

J. Clin. Invest.

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“…The in situ pH (pHi) at the base and tip collecting duct was determined with single or double barrelled glass membrane pH microelectrodes of 7-10 gm tip Diam as reported previously (18). Electrodes having a sensitivity of <57 mV/pH unit were not used.…”

Section: Microelectrode Techniquesmentioning

confidence: 99%

“…Therefore, most of the in situ pH data were obtained with single-barrelled electrodes because of ease of construction. Calibration before and after in vivo use was as described previously (16,18).…”

Section: Microelectrode Techniquesmentioning

confidence: 99%

“…The equilibrium pH (pHq) was measured in vivo with a composite probe consisting of an aspiration pipette into which a single-barrelled pH electrode was inserted. This electrode was designed and constructed in our laboratory and has been described in detail (18). This electrode consists of an outer shell (aspiration or collection pipette) of borosilicate glass capillary (2 mm) that was pulled to a taper length of 6-7 mm and beveled at a 50-60°angle to an outer tip Diam of 4-9 Mm.…”

Section: Microelectrode Techniquesmentioning

confidence: 99%

“…The disequilibrium pH method (pHdq = pHi, -pHeq) has been used by several investigators to demonstrate delayed dehydration, and thus H+ secretion in other nephron segments (18,19). Recently, we have used newly developed microelectrode techniques to measure Pco2, in situ pH (pHij), and equilibrium pH (pHeq).…”

Section: Introductionmentioning

confidence: 99%

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Hydrogen ion secretion by the collecting duct as a determinant of the urine to blood PCO2 gradient in alkaline urine.

DuBose¹

1982

J. Clin. Invest.

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A B S T R A C T Several theories have been advanced to explain the elevation in urinary Pco2 during bicarbonate loading and include: (a) H+ secretion, (b) countercurrent system for CO2, (c) the "ampholyte" properties of bicarbonate, and (d) mixing of urine of disparate bicarbonate and buffer concentrations. In this study microelectrodes were used to measure in situ and equilibrium pH (pHi, and pHeq) and Pco2 in control and bicarbonate loaded rats before and after infusion of carbonic anhydrase. The disequilibrium pH method (pHdq = pHi, -pHeq) was used to demonstrate H+ secretion. Control rats excreting an acid urine (pH = 6.04±0.06) failed to display a significant disequilibrium pH at the base (BCD), or tip (TCD) of the papillary collecting duct. Urine pH (7.54±0.12), and urine to blood (U-B) Pco2 increased significantly during NaHCO3 loading while Pco2 at the BCD and TCD also increased (95±4 and 122±4). Furthermore, an acid disequilibrium pH was present at both the BCD and TCD (-0.42±0.04 and -0.36±0.03) and was obliterated by carbonic anhydrase. Comparison of the Pco2 in the BCD or TCD with the adjacent vasa recta revealed similar values (r = 0.97). It is concluded that H+ secretion by the collecting duct into bicarbonate containing fluid with delayed dehydration of H2CO3, is the most likely determinant of the U-B Pco2 in alkaline urine. Similar values for Pco2 in the collecting

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Molecular Mechanisms and Regulation of Urinary Acidification

Kurtz

2014

Comprehensive Physiology

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The H+ concentration in human blood is kept within very narrow limits, ~ 40 nM, despite the fact that dietary metabolism generates acid and base loads that are added to the systemic circulation throughout the life of mammals. One of the primary functions of the kidney is to maintain the constancy of systemic acid-base chemistry. The kidney has evolved the capacity to regulate blood acidity by performing three key functions: 1) reabsorb HCO3− that is filtered through the glomeruli to prevent its excretion in the urine; 2) generate a sufficient quantity of new HCO3− to compensate for the loss of HCO3− resulting from dietary metabolic H+ loads and loss of HCO3− in the urea cycle; and 3) excrete HCO3− (or metabolizable organic anions) following a systemic base load. The ability of the kidney to perform these functions requires that various cell types throughout the nephron respond to changes in acid-base chemistry by modulating specific ion transport and/or metabolic processes in a coordinated fashion such that the urine and renal vein chemistry is altered appropriately. The purpose of the article is to provide the interested reader with a broad review of a field that began historically ~ 60 years ago with whole animal studies, and has evolved to where we are currently addressing questions related to kidney acid-base regulation at the single protein structure/function level.

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Determination of disequilibrium pH in the rat kidney in vivo: evidence of hydrogen secretion

Cited by 33 publications

References 0 publications

Contribution of individual superficial nephron segments to ammonium handling in chronic metabolic acidosis in the rat. Evidence for ammonia disequilibrium in the renal cortex.

Contribution of individual superficial nephron segments to ammonium handling in chronic metabolic acidosis in the rat. Evidence for ammonia disequilibrium in the renal cortex.

Hydrogen ion secretion by the collecting duct as a determinant of the urine to blood PCO2 gradient in alkaline urine.

Molecular Mechanisms and Regulation of Urinary Acidification

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