Load dependence of proximal tubular fluid and bicarbonate reabsorption in the remnant kidney of the Munich-Wistar rat.

Maddox, David A.; Horn, Johanna; Famiano, F C; Gennari, F. John

doi:10.1172/jci112481

Cited by 26 publications

(15 citation statements)

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“…Abbreviations used in this paper: Al,, angiotensin II; APRHco,, proximal tubular bicarbonate reabsorptive rate; ARHcO3, whole-kidney bicarbonate reabsorptive rate; FLHCo3 filtered load of bicarbonate; Hct, hematocrit. the glomerulus, thereby effectively increasing the length of the proximal tubule that can participate in bicarbonate reabsorption (1). Delivery-dependent changes in bicarbonate reabsorption occur both in the early and the late proximal tubule, although the capacity to increase reabsorption is much greater in the early proximal tubule (7)(8)(9)(10)(11). Although an increase in FLHco, induced by acute plasma expansion increases both early and late proximal bicarbonate reabsorption, no evidence of a decrease in the fraction of bicarbonate reabsorbed by the early proximal tubule is observed (7,12,13), as would be expected if luminal pH and/or bicarbonate concentration gradients were the controlling factor.…”

Section: Introductionmentioning

confidence: 99%

Effect of acute changes in glomerular filtration rate on Na+/H+ exchange in rat renal cortex.

Maddox

Fortin²,

Tartini³

et al. 1992

J. Clin. Invest.

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Studies were undertaken in Munich-Wistar rats to assess the influence of changes in filtered bicarbonate (FLHCo), induced by changes in GFR, on Na+/H' exchange activity in renal brush border membrane vesicles (BBMV). Whole-kidney and micropuncture measurements of GFR, FLHco3, and whole-kidney and proximal tubule HCO3 reabsorption (APRHCo) were coupled with BBMV measurements of H' gradient-driven 22Na' uptake in each animal studied. 22Na' uptake was measured at three Na' concentration gradients to allow calculation of V., and K. for Na+/H' exchange. GFR was varied by studying animals under conditions of hydropenia, plasma repletion, and acute plasma expansion. The increase in GFR, FLHco3, and APRHco3 induced by plasma administration correlated directly with an increase in the V.,, for Na+/H' exchange in BBMV.The K,. for sodium was unaffected. In the plasma-expanded rats, the V. for Na+/H' exchange was 22% greater than in the hydropenic rats (P < 0.025) whereas APRHco3 was 86% greater (P < 0.001). These results indicate that increases in FLHCo3, induced by acute increases in GFR, stimulate Na+/H' exchange activity in proximal tubular epithelium. This stimulation is a mechanism which can, in part, account for the delivery dependence of proximal bicarbonate reabsorption. (J. Clin. Invest. 1992Invest. . 89:1296Invest. -1303

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Section: Introductionmentioning

confidence: 99%

Effect of acute changes in glomerular filtration rate on Na+/H+ exchange in rat renal cortex.

Maddox

Fortin²,

Tartini³

et al. 1992

J. Clin. Invest.

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“…In two other studies in humans, serum [total CO 2 ] did not increase significantly after a 50% reduction in protein, but both studies contained very few subjects (10,11). The best data supporting an effect of protein restriction on body alkali stores in CKD come from a partial nephrectomy rat model (12). In this model, steady-state serum [HCO 3 Ϫ ] was significantly higher (by 2 mEq/L) in animals that ingested a low-protein diet (6% of total calories/d) as compared with animals that ingested a normal-protein diet (24% of total calories/d).…”

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confidence: 97%

Effect of Dietary Protein Intake on Serum Total CO2 Concentration in Chronic Kidney Disease

Gennari

Hood

Greene

et al. 2006

Clinical Journal of the American Society of Nephrology

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Metabolic acidosis is a feature of chronic kidney disease (CKD), but whether serum bicarbonate concentration is influenced by variations in dietary protein intake is unknown. For assessing the effect of diet, data that were collected in the Modification of Diet in Renal Disease study were used. In this study, patients with CKD were enrolled into a baseline period, then randomly assigned to follow either a low-or a usual-protein diet (study A, entry GFR 25 to 55 ml/min) or a low-or very low-protein diet, the latter supplemented with ketoanalogs of amino acids (study B, entry GFR 13 to 24 ml/min). Serum [total CO 2 ] and estimated protein intake (EPI) were assessed at entry (n ‫؍‬ 1676) and again at 1 yr after randomization, controlling for changes in GFR and other key covariates (n ‫؍‬ 723 ]) falls as GFR decreases in chronic kidney disease (CKD) (1,2), but the values vary widely among patients with similar levels of kidney function. Part of this difference may be due to dietinduced differences in endogenous acid production. In individuals with normal kidney function, the effect of diet on serum [total CO 2 ] is small and not detectable unless the influence of Paco 2 is removed (3). Given the impairment in acid excretion that occurs in CKD (4 -6), one might anticipate that differences in diet-induced acid production would have a greater influence on serum [total CO 2 ] than in people with normal kidney function. The major source of endogenous acid production comes from metabolism of dietary protein (7); therefore, protein restriction should result in an increase in serum [total CO 2 ] if this hypothesis is correct. Despite extensive studies on the effects of protein restriction on metabolic parameters and kidney disease progression (8), little attention has been directed to the effect of this intervention on serum [total CO 2 ] in CKD. In one study in humans with severe CKD, serum [HCO 3 Ϫ ] was notably higher when the patients were compliant with a very low-protein diet (0.3 g/kg body weight) supplemented with ketoanalogs of amino acids (9). In two other studies in humans, serum [total CO 2 ] did not increase significantly after a 50% reduction in protein, but both studies contained very few subjects (10,11). The best data supporting an effect of protein restriction on body alkali stores in CKD come from a partial nephrectomy rat model (12). In this model, steady-state serum [HCO 3 Ϫ ] was significantly higher (by 2 mEq/L) in animals that ingested a low-protein diet (6% of total calories/d) as compared with animals that ingested a normal-protein diet (24% of total calories/d).To determine whether systematic changes in dietary protein intake affect serum [total CO 2 ] in a large cohort of patients with CKD, we evaluated the data collected in patients who participated in the Modification of Diet in Renal Disease (MDRD) study, focusing on GFR, protein intake, and serum [total CO 2 ] (13). Our analysis demonstrates that [total CO 2 ] is inversely related to dietary protein intake in this group of patients and that...

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“…In fact, at the highest delivery rates (2,100-2,500 pmol/min), proximal bicarbonate reabsorption is lower in respiratory acidosis than in normocapneic remnant kidney rats. The rats in this latter group have proximal tubular hypertrophy (6), in contrast to the CRACID animals. Because we found no stimulation ofbicarbonate reabsorption at any given distance from Bowman's space in remnant kidney rats compared with two-kidney plasma expanded rats at similar FLHCo3 values (6), it seems unlikely that tubular hypertrophy is responsible for the higher rate of reabsorption.…”

Section: Experimental Protocolsmentioning

confidence: 86%

“…The first 1-2 mm ofthe proximal tubule ofthe rat nephron is a high capacity site for bicarbonate reabsorption, normally recapturing some 50-60% of filtered bicarbonate (1)(2)(3)(4)(5)(6)(7)(8). Bicarbonate reabsorption at this site in the nephron, moreover, varies in direct relation to the filtered or perfused load over a wide range of loads (2,(4)(5)(6)(7)(8)(9)(10).…”

Section: Introductionmentioning

confidence: 99%

“…Bicarbonate reabsorption at this site in the nephron, moreover, varies in direct relation to the filtered or perfused load over a wide range of loads (2,(4)(5)(6)(7)(8)(9)(10). In addition to delivery, a variety of studies of bicarbonate transport in isolated tubule segments in vivo or in vitro have shown that acidosis stimulates and alkalosis inhibits proximal bicarbonate reabsorption (11)(12)(13)(14)(15)(16).…”

Section: Introductionmentioning

confidence: 99%

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Delivery dependence of early proximal bicarbonate reabsorption in the rat in respiratory acidosis and alkalosis.

Santella¹,

Maddox²,

Gennari³

1991

J. Clin. Invest.

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In the intact rat kidney, bicarbonate reabsorption in the early proximal tubule (EP) is strongly dependent on delivery. Independent ofdelivery, metabolic acidosis stimulates EP bicarbonate reabsorption. In this study, we investigated whether systemic pH changes induced by acute or chronic respiratory acidbase disorders also affect EP HCO3 reabsorption, independent of delivery (FLHCO3, filtered load of bicarbonate). Hypercapnia was induced in rats acutely (1-3 h) and chronically (4-5 d) by increasing inspired Pco2. Hypocapnia was induced acutely (1-3 h) by mechanical hyperventilation, and chronically (4-5 d) using hypoxemia to stimulate ventilation. When compared with normocapneic rats with similar FLHco3, no stimulation of EP or overall proximal HCO3 reabsorption was found with either acute hypercapnia (Pac = 74 mmHg, pH = 7.23) or chronic hypercapnia (Pa<> = 84 mmHg, pH = 7.31). Acute hypocapnia (Pac, = 29 mmHg, pH = 7.56) did not suppress EP or overall HC03 reabsorption. Chronic hypocapnia (Pa2 = 26 mmHg, pH = 7.54) reduced proximal HCO3 reabsorption, but this effect was reversed when FLHCo3 was increased to levels comparable to euvolemic normocapneic rats. Thus, when delivery is accounted for, we could find no additional stimulation of proximal bicarbonate reabsorption in respiratory acidosis and, except at low delivery rates, no reduction in bicarbonate reabsorption in respiratory alkalosis. (J. Clin. Invest. 1991. 87:631-638.)

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Load dependence of proximal tubular fluid and bicarbonate reabsorption in the remnant kidney of the Munich-Wistar rat.

Abstract: Studies were undertaken to characterize the pattern of proximal tubular fluid (APRHIO) and bicarbonate reabsorption (APRHCO,)

Cited by 26 publications

References 27 publications

Effect of acute changes in glomerular filtration rate on Na+/H+ exchange in rat renal cortex.

Effect of acute changes in glomerular filtration rate on Na+/H+ exchange in rat renal cortex.

Effect of Dietary Protein Intake on Serum Total CO2 Concentration in Chronic Kidney Disease

Delivery dependence of early proximal bicarbonate reabsorption in the rat in respiratory acidosis and alkalosis.

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