Kidney oxygen consumption, carbonic anhydrase, and proton secretion

2006 ◽  
Vol 290 (5) ◽  
pp. F1009-F1015 ◽  
Author(s):  
Aihua Deng ◽  
Cynthia M. Miracle ◽  
Mark Lortie ◽  
Joseph Satriano ◽  
Francis B. Gabbai ◽  
...  
Keyword(s):  
Carbonic Anhydrase ◽  
Proximal Tubule ◽  
Hydrogen Exchange ◽  
Chloride Transport ◽  
Sodium Reabsorption ◽  
Sodium Hydrogen ◽  
Adenosine A1 ◽  
A1 Receptor ◽  
Relationship Of ◽  
The Relationship

Oxygen consumed by the kidney (QO2) is primarily obligated to sodium reabsorption (TNa). The relationship of QO2 to TNa (QO2/TNa) may be altered by hormones and autacoids. To examine whether QO2/TNa depends on the mechanism of sodium reabsorption, we first evaluated the effects on QO2 and QO2/TNa of benzolamide (BNZ), a proximal diuretic that works by inhibiting membrane carbonic anhydrase. During BNZ infusion in anesthetized rats, QO2 increased by 50% despite a 25% decline in TNa. However, BNZ failed to increase QO2/TNa when given along with the adenosine A1 receptor blocker, DPCPX, which inhibits basolateral Na-bicarbonate cotransport (NBC1), or EIPA, which inhibits sodium-hydrogen exchange (NHE). Incubating freshly harvested rat proximal tubules with BNZ also caused QO2to increase by 62%, an effect that was prevented by blocking the apical NHE3 with S3226. Blocking NBC1 or NHE3 in the proximal tubule will have opposite effects on cell pH, but both maneuvers should reduce active chloride transport. In conclusion, inhibiting membrane carbonic anhydrase in the proximal tubule increases QO2 and reduces the energy efficiency of sodium reabsorption by the kidney. This is not purely due to shifting the burden of reabsorption to a more expensive site downstream from the proximal tubule. Instead, increased cost may be incurred within the proximal tubule as the result of increased active chloride transport.

Insulin-like growth factor I stimulates apical sodium/hydrogen exchange in human proximal tubule cells

1997 ◽  
Vol 272 (4) ◽  
pp. F484-F490 ◽  
Author(s):  
D. W. Johnson ◽  
B. K. Brew ◽  
P. Poronnik ◽  
D. I. Cook ◽  
M. J. Field ◽  
...  
Keyword(s):  
Growth Factor ◽  
Proximal Tubule ◽  
Hydrogen Exchange ◽  
Insulin Like Growth Factor ◽  
Proximal Tubule Cells ◽  
Factor I ◽  
Sodium Hydrogen ◽  
Igf I ◽  
Tubule Cells ◽  
Stimulation Of

To determine whether insulin-like growth factor I (IGF-I) stimulated apical sodium/hydrogen exchange (NHE), confluent primary human proximal tubule cells (PTC) were incubated for 48 h in serum-free media in the presence or absence of 100 ng/ml IGF-I. Cells incubated in IGF-I demonstrated significant increases in thymidine incorporation (181.2 +/- 30.3% of control values; n = 12, P = 0.01) and in resting intracellular pH (pHi) (7.52 +/- 0.08 vs. 7.30 +/- 0.06; n = 20, P < 0.05), as determined by 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein quantitative microspectrofluorometry. Following intracellular acid loading, ethylisopropylamiloride (EIPA)-inhibitable H+ efflux and 22Na+ influx after 1 min were both significantly enhanced in IGF-I-treated cells compared with controls (8.78 +/- 1.69 vs. 3.03 +/- 0.72 mM/min and 3.47 +/- 0.49 vs. 1.55 +/- 0.35 nmol x mg protein(-1) x min(-1), respectively). 22Na+ uptake studies in PTC grown on permeable supports demonstrated preferential stimulation of apical vs. basolateral NHE. The 50% inhibitory concentrations (IC50) in IGF-I-treated and control cells for EIPA (0.5 and 1.1 microM, respectively) and for HOE-694 (4.0 and 10.0 microM, respectively) were also consistent with predominant activation of apical, rather than basolateral, NHE activity. Kinetic analysis revealed an increase in maximal transport velocity (Vmax, 15.50 +/- 1.50 vs. 7.26 +/- 3.07 mM/min; n = 10, P < 0.05), without a significant change in antiporter affinity for extracellular Na+. Incubation of PTC with 100 ng/ml IGF-I produced an acute, reversible, and EIPA-inhibitable pHi increase of 0.05 +/- 0.01 pH units (n = 5, P < 0.05). The results suggest that IGF-I may contribute to the metachronous stimulation of apical NHE and PTC growth observed in many physiological and pathological conditions involving the human kidney.

scholarly journals Peroxisome development in the metanephric kidney of mouse.

1975 ◽  
Vol 23 (12) ◽  
pp. 957-973 ◽  
Author(s):  
J A Goeckermann ◽  
E L Vigil
Keyword(s):  
Proximal Tubule ◽  
Specific Activity ◽  
Postnatal Growth ◽  
Acid Oxidase ◽  
Amino Acid Oxidase ◽  
Voltage Electron ◽  
Metanephric Kidney ◽  
Biochemical Analyses ◽  
Relationship Of ◽  
The Relationship

The relationship of enzymatic activity to organelle development and organelle number during differentiation of the metanephric kidney in the mouse was approached from several experimental directions. Biochemical analyses of marker enzymes for peroxisomes (catalase and D-amino acid oxidase), mitochondria (cytochrome oxidase) and lysosomes (acid phosphatase) were performed on kidneys at ages from 17 days prenatal to adult. These data were correlated with a morphometric analysis of populations of peroxisomes and mitochondria in differentiating cells of the proximal tubule. Postnatal development of the metanephric kidney was found to be accompanied by a rapid increase in both the specific activity of catalase and the number of peroxisomes per 100 mu2 in the proximal tubule during the first 4 weeks of postnatal growth. Elaboration of the endoplasmic reticulum (ER) was seen to parallel the increase in number of peroxisomes to which segments of ER were often in close apposition. Extensive interactions between segments of ER and peroxisomes were readily visible in 0.5-mu sections viewed in the high voltage electron microscope. In contrast to peroxisomes, neither mitochondria nor lysosomes followed a similar pattern of net organelle increase, suggesting that a defined population density of mitochondria and lysosomes may exist in the proximal tubule at birth, prior to complete development of the kidney.

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