Transport of citrate across renal brush border membrane: effects of dietary acid and alkali loading

Jenkins, Alan D.; Douša, Thomas P.; Smith, Lynwood H.

doi:10.1152/ajprenal.1985.249.4.f590

Cited by 56 publications

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“…Transport measurements were determined by the Millipore rapid membrane filtration technique 22,23) . For the experimentsin which BBMV were incubated with CoCl 2 or NiCl 2 , membrane vesicles (10 µl) were incubated at 30°C with 10 µ of incubation solution consisting of 260 mM mannitol, 20 mM HEPES/Tris, pH7.0, with CoCl 2 or NiCl 2 .…”

Section: Citrate Uptakementioning

confidence: 99%

Direct Effect of CoCl2 and NiCl2 on Citrate Uptake by the Rat Renal Brush Border Membrane

et al. 2005

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Co and Ni are essential but relatively rare elements as to organisms. In the mammalian membrane, these metals are transported by the same carrier proteins. The aim of this study was to investigate the direct effects of CoCl 2 and NiCl 2 on citrate uptake by rat renal brush border membrane vesicles (BBMV). BBMV were prepared by the divalent cation precipitation methods, and citrate uptake was measured by the Millipore rapid membrane filtration technique. The time course of citrate uptake during 120-min of incubation with 1 mM CoCl 2 and NiCl 2 showed a rapid significant inhibition at the early phase and a slight recover at the late phase. Incubation for 1 min of BBMV with 1, 5 and 25 mM CoCl 2 and NiCl 2 , respectively, significantly inhibited citrate uptake in a concentration-dependent manner compared with that of 0 mM. We discuss these findings from the point of view that Co and Ni are located in Group VIII of the periodic table.

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Section: Citrate Uptakementioning

confidence: 99%

Direct Effect of CoCl2 and NiCl2 on Citrate Uptake by the Rat Renal Brush Border Membrane

et al. 2005

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“…Since citrate uptake is sodium dependent and electrogenic, positive charge is transported 12) , transport measurements were determined by the Millipore rapid membrane filtration technique [13][14][15] . In a typical uptake experiment, BBMV (10 µl) were incubated at 30°C with 40 µl of uptake solution consisting of 100 µM 14 C-citrate, 130 mM NaCl or KCl and 20 mM HEPES/Tris, pH 7.0.…”

Section: Uptake Studiesmentioning

confidence: 99%

“…All uptake measurements were performed at 30°C in triplicate, and uptake was calculated on the basis of the specific activity measured in each experiment. The value of non-specific binding was subtracted from the experimental value, and the vesicular uptake was expressed as picomoles 14 C-citrate per mg protein.…”

Section: Uptake Studiesmentioning

confidence: 99%

Effect of Platinum Coordination Complex (PtCx) on Citrate Uptake by Rat Renal Brush Border Membrane Vesicles (BBMV): Cisplatin-Intoxicated Rats.

et al. 2001

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Platinosis with severe dermatitis and/or asthma is broadly defined as the effects of soluble platinum salts on people exposed to them occupationally. Platinum coordination complexes are widely used in the treatment of a variety of solid tumors. However, the clinical use of cisplatin, the most useful agent, is limited by the development of nephrotoxicity. Thus, an accidental exposure to soluble platinum at a high dose in platinum refineries and pharmaceutical factories could induce occupational nephrotoxicity. Urinary citrate is freely filtered at the glomerulus, and its reabsorption in the proximal tubule is the major determinant of the rate of renal excretion. In our previous studies, we found that the preincubation of rat renal brush border membrane vesicles (BBMV) with cisplatin and carboplatin, a second-generation platinum coordination complex, significantly inhibited the citrate uptake compared with that of the control BBMV. In this study, we performed in vivo expriments in cisplatin-intoxicated rats to elucidate the toxic mechanism of cisplatin. And our results showed that the citrate uptake was significantly inhibited in cisplatin-intoxicated rats at 1 min compared with that of control rats.

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“…For example, the suppression of proximal phosphate and enhanced citrate absorption occur by different mechanisms with chronic metabolic acidosis compared with acute decreases of luminal pH. 42,43 There are a multitude of genes and gene products that are regulated by chronic systemic metabolic acidosis in the kidney. Table 2 summarizes some of the studies of adaptation of renal metabolism and transport in chronic metabolic acidosis and aims to highlight rather than provide an exhaustive catalogue.…”

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confidence: 99%

Na+/H+ Exchangers in Renal Regulation of Acid-Base Balance

Bobulescu

Moe

2006

Seminars in Nephrology

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The kidney plays key roles in extracellular fluid pH homeostasis by reclaiming bicarbonate (HCO 3 − ) filtered at the glomerulus and generating the consumed HCO 3 − by secreting protons (H + ) into the urine (renal acidification). Sodium-proton exchangers (NHEs) are ubiquitous transmembrane proteins mediating the countertransport of Na + and H + across lipid bilayers. In mammals, NHEs participate in the regulation of cell pH, volume, and intracellular sodium concentration, as well as in transepithelial ion transport. Five of the 10 isoforms (NHE1-4 and NHE8) are expressed at the plasma membrane of renal epithelial cells. The best-studied isoform for acid-base homeostasis is NHE3, which mediates both HCO 3 − absorption and H + excretion in the renal tubule. This article reviews some important aspects of NHEs in the kidney, with special emphasis on the role of renal NHE3 in the maintenance of acid-base balance.Keywords sodium/hydrogen exchange; renal acidification; bicarbonate absorption The free hydrogen ion (H + ) concentration in body fluids is regulated exquisitely around 40 nmol/L (pH 7.40) whereas H + flux through the body greatly exceeds this magnitude. In a 70-kg human being at a basal state, normal metabolic and dietary acid production rate is about 50 to 70 mmoles/d and respiratory volatile acid production at the basal state is around 15,000 mmoles/d, with peak production at maximal exercise reaching 200 mmoles/min. The flux of H + through the organism over 24 hours is 8 orders of magnitude greater than the total pool of free H + in total body water (<2 μmoles). This remarkable homeostatic feat is accomplished by concerted efforts of extracellular and intracellular buffers, highly efficient ventilatory responses, metabolic functions of the liver, and renal ammoniagenic and solute transport mechanisms. For excretion of nonvolatile acid and base loads, the kidney assumes the pivotal role.A filtration-reabsorption nephron bears an exorbitant burden of having to reclaim a vast amount of valuable solutes indiscriminately dispensed in the filtrate; one of which of course is the approximately 4,000 mmoles of bicarbonate (HCO 3 − ) per day. The luminal acid disequilibrium pH implies that the predominant mode of HCO 3 − absorption involves H + secretion, although a small concomitant degree of direct HCO 3 − reabsorption cannot be excluded. 1 Two points are noteworthy. First, complete reclamation of the approximately 4,000 mmoles of filtered HCO 3 − forestalls a physiologic disaster but does not lead to net acid secretion. Further elaboration of H + into the urine is necessary. Second, whether the organism is catering to the The era of phenomenologic analysis was supplemented by gene-and protein-specific reagents when the first mammalian NHE was cloned by Sardet et al. 7 The relationship between mammalian NHE genetic sequence and those from a multitude of organisms is shown in Fig 2. Na + /H + exchange across lipid bilayers and proteins that sustain this function are universal in prokaryotic, animal, and...

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Transport of citrate across renal brush border membrane: effects of dietary acid and alkali loading

Cited by 56 publications

References 0 publications

Direct Effect of CoCl2 and NiCl2 on Citrate Uptake by the Rat Renal Brush Border Membrane

Direct Effect of CoCl2 and NiCl2 on Citrate Uptake by the Rat Renal Brush Border Membrane

Effect of Platinum Coordination Complex (PtCx) on Citrate Uptake by Rat Renal Brush Border Membrane Vesicles (BBMV): Cisplatin-Intoxicated Rats.

Na+/H+ Exchangers in Renal Regulation of Acid-Base Balance

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