Zur Technik und Spezifit�t des histochemischen Carboanhydrasenachweises im Modellversuch und in Gewebsschnitten von Rattennieren

Häusler, G.

doi:10.1007/bf00736626

Cited by 109 publications

(19 citation statements)

References 13 publications

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“…Histochemical studies confirmed this proximal luminal CA activity and furthermore demonstrated intracellular CA activity in both the proximal and distal tubule (15 …”

Section: Discussionsupporting

confidence: 57%

Enzymatically Inactive Red Cell Carbonic Anhydrase B in a Family with Renal Tubular Acidosis

Shapira¹,

Ben‐Yoseph²,

Eyal³

et al. 1974

J. Clin. Invest.

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“…Histochemical studies confirmed this proximal luminal CA activity and furthermore demonstrated intracellular CA activity in both the proximal and distal tubule (15 …”

Section: Discussionsupporting

confidence: 57%

Enzymatically Inactive Red Cell Carbonic Anhydrase B in a Family with Renal Tubular Acidosis

Shapira¹,

Ben‐Yoseph²,

Eyal³

et al. 1974

J. Clin. Invest.

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“…Analyses of isolated tubules by Kark and his colleagues (26) for carbonic anhydrase activity, as well as histochemical stains for enzyme activity (27), have shown the enzyme to be present in both proximal and distal portions of the nephron. The histochemical staining, however, which is dependent on the precipitation of CoCO3 at sites of enzymatic activity, with subsequent conversion to CoS, gives different patterns in proximal and distal tubules (27).…”

Section: Discussionmentioning

confidence: 99%

“…The histochemical staining, however, which is dependent on the precipitation of CoCO3 at sites of enzymatic activity, with subsequent conversion to CoS, gives different patterns in proximal and distal tubules (27). In the proximal tubule there is dense localization of enzyme along the peritubular membrane with less intense activity throughout the remainder of the cellular cytoplasm; in addition, there is precipitation of CoS in the tubular lumen, suggesting that the tubular fluid is exposed to enzymatic activity.…”

Section: Discussionmentioning

confidence: 99%

The Mechanism of Bicarbonate Reabsorption in the Proximal and Distal Tubules of the Kidney*

Rector¹,

Carter²,

Seldin³

1965

J. Clin. Invest.

277

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Considerable evidence (1-6) has been adduced to support the hypothesis that the reabsorption of filtered HCO3-by the kidney is mediated by a single mechanism, operative in both the proximal and distal portions of the nephron, which involves the secretion of cellular He in exchange for luminal Na+. The secreted Ho reacts with filtered HC03-to form H2CO3, which then decomposes to C02 and H20.Difficulties arise, however, when the details of the process are examined. In the steady state, the rate at which the H2CO3 is removed from the luminal fluid must equal the rate at which H+ is secreted. Walser and Mudge (7) have estimated that for the uncatalyzed dehydration of H2C03 to account for the observed rates of HC03-reabsorption, the steady-state concentration of H2C03 in luminal fluid must be at least tenfold greater than the concentration that would exist were H2C03 in equilibrium with the C02 tension of luminal fluid and plasma. As a result of the excess H2C03, the steady-state pH would be approximately 1 pH U lower than would be predicted from the luminal concentration of HC03-and the C02 tension of plasma, assuming complete equilibration of luminal H2C03 with plasma C02. A marked disequilibrium pH ' would exist.Two lines of evidence have been advanced to support the presence of a disequilibrium pH in the proximal tubule. Rector and Carter (8) perfused single proximal tubules with NaHCO3 * Submitted for publication July 27, 1964; accepted October 29, 1964. Supported in part by a grant from the American Heart Association and in part by grants 5 TI AM-5028 and 5 TI HE-5469 from the National Institutes of Health.'The difference between the actual pH, under conditions where C02 and H2CO0 are not in equilibrium, and the calculated equilibrium pH will be termed "disequilibrium" pH. and estimated the steady-state intraluminal pH from the change in color of various acid-base indicators. The pH was found to be about 1.5 U lower than the predicted equilibrium pH. However, since the color change could result from loss of dyes by either reabsorption or binding to cell proteins, the validity of these results may be questioned. Bank and Aynedjian (9) measured intratubular pH by aspirating tubular fluid into quinhydrone microelectrodes and comparing the readings while the electrode was still in the tubular lumen with the values obtained when the fluid was removed from the tubule and permitted to reach equilibrium. With this technique, they found the intratubular pH to be 2.0 to 2.5 pH U below the equilibrium pH. These results, however, are open to the serious objection that a disequilibrium pH of this magnitude would require the generation of H2CO3 at a rate 10 to 50 times greater than is theoretically possible, as judged from the rate of HC03-reabsorption.The presence of a disequilibrium pH, however, is not a necessary consequence of the hypothesis that H+ secretion mediates HC03-reabsorption. An equilibrium pH could obtain if H2CO3 were rapidly removed from the tubular urine by either of two mechanisms: 1) nonionic diffusion...

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“…(c) The lower urinary tract must be relatively impermeable to carbon dioxide formed in this way. There are numerous reports in the literature to support these criteria (8)(9)(10)(11)(12). Therefore urinary Pco2 levels could provide a qualitative index for collecting duct hydrogen-ion secretion.…”

Section: Introductionmentioning

confidence: 97%

Studies on the Pathogenesis of Type I (Distal) Renal Tubular Acidosis as Revealed by the Urinary Pco2 Tensions

Ml¹,

Goldstein²,

Haig³

et al. 1974

J. Clin. Invest.

181

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Zur Technik und Spezifit�t des histochemischen Carboanhydrasenachweises im Modellversuch und in Gewebsschnitten von Rattennieren

Cited by 109 publications

References 13 publications

Enzymatically Inactive Red Cell Carbonic Anhydrase B in a Family with Renal Tubular Acidosis

Enzymatically Inactive Red Cell Carbonic Anhydrase B in a Family with Renal Tubular Acidosis

The Mechanism of Bicarbonate Reabsorption in the Proximal and Distal Tubules of the Kidney*

Studies on the Pathogenesis of Type I (Distal) Renal Tubular Acidosis as Revealed by the Urinary Pco2 Tensions

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