Na-HCO3 cotransport and Na-H antiporter in chronic respiratory acidosis and alkalosis

1989 ◽  
Vol 256 (3) ◽  
pp. F414-F420 ◽  
Author(s):  
O. S. Ruiz ◽  
J. A. Arruda ◽  
Z. Talor
Keyword(s):  
Proximal Tubule ◽  
Respiratory Acidosis ◽  
Renal Proximal Tubule ◽  
Transport Systems ◽  
Acid Base ◽  
Basolateral Membranes ◽  
Two Systems ◽  
22Na Uptake ◽  
And Control

Renal acidification in renal proximal tubule is thought to be mediated by luminal Na-H antiporter and the HCO3- generated by this antiporter is removed from the cell by a basolateral Na-HCO3 cotransporter. To study the effect of respiratory acid-base disorders on these transport systems, we have measured the Na-HCO3 cotransport in basolateral membranes and Na-H antiporter in luminal membranes in control rabbits, rabbits exposed to 10% CO2 (chronic hypercapnia), and rabbits exposed to 10% O2-90% N2 (chronic hypocapnia). The Vmax of HCO3(-)-dependent 22Na uptake was significantly higher in chronic hypercapnia than controls (2.54 +/- 0.03 vs. 1.18 +/- 0.21 nmol.mg protein-1.3 s-1, P less than 0.001). Likewise, the Vmax of the Na-H antiporter was also increased compared with controls (924.9 +/- 42.1 vs. 549.1 +/- 62.8 fluorescence units (FU).300 micrograms protein-1.min-1). In chronic hypocapnia, the Vmax of Na-HCO3 cotransport was lower than controls (0.72 +/- 0.11 vs. 1.18 +/- 0.21 nmol.mg protein-1.3 s-1, P less than 0.05). There was no difference, however, in the Vmax of the Na-H antiporter between hypocapnia and control (524.2 +/- 24.3 vs. 549.1 +/- 62.8, FU.300 micrograms protein-1.min-1). The Vmaxs of the Na-HCO3 cotransport and of the Na-H antiporter in hypocapnic, control, and hypercapnic rabbits were linearly related (r = 0.81), suggesting a simultaneous adaptation of the two systems in respiratory acid-base disorders.(ABSTRACT TRUNCATED AT 250 WORDS)

Interactions between gluconeogenesis and sodium transport in rabbit proximal tubule

1984 ◽  
Vol 246 (6) ◽  
pp. F859-F869 ◽  
Author(s):  
S. R. Gullans ◽  
P. C. Brazy ◽  
V. W. Dennis ◽  
L. J. Mandel
Keyword(s):  
Proximal Tubule ◽  
Sodium Transport ◽  
Acid Metabolism ◽  
Renal Proximal Tubule ◽  
Active Sodium ◽  
Atp Production ◽  
Cellular Energy ◽  
Glucose Synthesis ◽  
And Control ◽  
Gluconeogenic Substrate

Gluconeogenesis and sodium transport are ATP-requiring functions of the renal proximal tubule. Previously observed interactions between these processes indicated that they may compete for cellular energy. We have reevaluated this interaction in the rabbit proximal tubule using two preparations: suspensions of cortical tubules and isolated perfused tubules. In the presence of lactate and alanine, net glucose synthesis was 22.3 +/- 1.3 nmol X mg protein-1 .30 min-1. Additions of valerate, butyrate, or succinate increased this rate by factors of 2-3 without affecting cellular ATP levels or net fluid absorption (Jv). Inhibition of ATP production with rotenone, which we have previously shown to inhibit Jv [Am. J. Physiol. 243 (Renal Fluid Electrolyte Physiol. 12): F133-F140, 1982], greatly decreased the gluconeogenic rate, but this was modulated by the type of gluconeogenic substrate used. Increasing Na-K-ATPase activity with nystatin or decreasing it with ouabain had widely differing effects, which also depended on the substrate regimen. We conclude that the interaction between gluconeogenesis and active sodium transport cannot be described by a simple competition for ATP. Rather, under normal circumstances, the renal proximal tubule can meet the energetic demands of both gluconeogenesis and sodium transport, and control of these processes is multifactorial and sensitive to fatty acid metabolism.

Effect of parathyroid hormone on acid/base transport in rabbit renal proximal tubule S3 segment

1993 ◽  
Vol 423-423 (1-2) ◽  
pp. 7-13 ◽  
Author(s):  
George Seki ◽  
Shigeo Taniguchi ◽  
Shu Uwatoko ◽  
Keiji Suzuki ◽  
Kiyoshi Kurokawa
Keyword(s):  
Parathyroid Hormone ◽  
Proximal Tubule ◽  
Renal Proximal Tubule ◽  
Acid Base ◽  
S3 Segment

Transepithelial sulfate transport by avian renal proximal tubule epithelium in primary culture

2002 ◽  
Vol 283 (6) ◽  
pp. R1354-R1361 ◽  
Author(s):  
Paul L. Dudas ◽  
J. Larry Renfro
Keyword(s):  
Proximal Tubule ◽  
Primary Cultures ◽  
Renal Proximal Tubule ◽  
Proximal Tubules ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Electrophysiological Properties ◽  
Ussing Chambers ◽  
And Control ◽  
Inorganic Sulfate

The mechanisms and control of transepithelial inorganic sulfate (Si) transport by primary cultures of chick renal proximal tubule monolayers in Ussing chambers were determined. The competitive anion, S2O3 2− (5 mM), reduced both unidirectional reabsorptive and secretory fluxes and net Sireabsorption with no effect on electrophysiological properties. The carbonic anhydrase (CA) inhibitor ethoxzolamide decreased net Si reabsorption ∼45%. CAII protein and activity were detected in isolated chick proximal tubules by immunoblots and biochemical assay, respectively. Cortisol reduced net Sireabsorption up to ∼50% in a concentration-dependent manner. Thyroid hormone increased net Si reabsorption threefold in 24 h, and parathyroid hormone (PTH) acutely stimulated net Sireabsorption ∼45%. These data indicate that CA participates in avian proximal tubule active transepithelial Si reabsorption, which cortisol directly inhibits and T3 and PTH directly stimulate.

Interactions of organic anions with the organic cation transporter in renal BBMV

1988 ◽  
Vol 254 (1) ◽  
pp. F56-F61 ◽  
Author(s):  
P. H. Hsyu ◽  
L. G. Gisclon ◽  
A. C. Hui ◽  
K. M. Giacomini
Keyword(s):  
Proximal Tubule ◽  
Organic Cation ◽  
Organic Anion ◽  
Organic Cation Transporter ◽  
Organic Anions ◽  
Renal Proximal Tubule ◽  
Ph Gradient ◽  
Transport Systems ◽  
Organic Cations ◽  
Initial Uptake

It is generally assumed that the organic cation transport system in the renal proximal tubule is specific for organic cations and the transport of organic cations is not affected by organic anions. However, there are also data in the literature demonstrating that probenecid, a classical inhibitor of organic anion transport systems, inhibits the transport of an organic cation, cimetidine, in the renal proximal tubule. In this study we investigated the effects of probenecid and furosemide on the transport of N'-methylnicotinamide (NMN) the classical substrate of the organic cation transporter, in brush-border membrane vesicles prepared from rabbit renal cortex. In the presence of a pH gradient, both probenecid (10 mM) and furosemide reduced the initial uptake of NMN. Probenecid reduced the initial uptake of NMN to 12.1% of the control values (1.19 +/- 0.26 pmol/mg) and furosemide reduced the initial uptake of NMN to 39.2%. Probenecid (10 mM) also decreased the initial transport of NMN in the absence of a pH gradient. Inhibition of the transport of NMN by probenecid was concentration dependent, with the concentration of probenecid resulting in 50% inhibition of the transport of NMN equal to 2.31 +/- 1.18 mM in the presence of a pH gradient. Probenecid appeared to be a competitive inhibitor of NMN transport. The apparent Km (mean +/- SE) of NMN transport (2.01 +/- 0.78 mM) was increased to 18.7 +/- 10 mM (P less than 0.05) by probenecid (10 mM), whereas the Vmax was not changed (125 +/- 19.2 pmol.s-1.mg-1 vs. 186 +/- 94 pmol.s-1.mg-1, P greater than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Basolateral sodium-coupled acid-base transport mechanisms of the rabbit proximal tubule

1989 ◽  
Vol 257 (5) ◽  
pp. F790-F797 ◽  
Author(s):  
J. Geibel ◽  
G. Giebisch ◽  
W. F. Boron
Keyword(s):  
Proximal Tubule ◽  
Time Course ◽  
Basolateral Membrane ◽  
Fluorescence Emission ◽  
Proximal Tubules ◽  
The Other ◽  
Transport Systems ◽  
Disulfonic Acid ◽  
Transport Mechanisms ◽  
Acid Base

We studied Na+-coupled acid-base transport at the basolateral membrane of single, isolated, perfused rabbit proximal tubules by monitoring the time course of intracellular pH (pHi). The latter was determined using a microspectrofluorometric apparatus to alternatively excite the pH-sensitive fluorescent dye 2',7'-bis-2-carboxyethyl-5(and -6)-carboxyfluorescein (BCECF) at 440 and 490 nm, while the fluorescence emission, was measured at 530 nm. All experiments were conducted in the nominal absence of HCO-3 S1, S2, and S3 segments from both superficial and juxtamedullary nephrons were examined individually. We found that removing Na+ from both the lumen and bath (i.e., basolateral solution) caused pHi to fall from 7.24 to 6.75 in the superficial S1 segment (SS1), from 7.14 to 6.67 in the SS2, and from 7.09 to 6.69 in the SS3. Similarly, in juxtamedullary nephrons (J), bilateral Na+ removal caused pHi to fall from 7.25 to 6.76 in the JS1, from 7.16 to 6.71 in the JS2, and from 7.10 to 6.75 in the JS3. In all six proximal tubule subtypes, returning Na+ to the bath caused pHi to recover (i.e., increase). 4,4'-Diisothiocyanostilbene-2,2'-disulfonic acid (DIDS, 50 microM), an inhibitor of HCO-3 transport systems, blocked this Na+-dependent pHi recovery in all three superficial subtypes and the JS3 but had no effect in either the JS1 or JS2. On the other hand, 50 microM ethylisopropyl amiloride (EIPA), an inhibitor of Na-H exchange, blocked the Na+-dependent pHi recovery in the JS1 and JS2 but had no effect in the JS3 or any of the superficial subtypes.(ABSTRACT TRUNCATED AT 250 WORDS)

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