Abstract
The present study evaluates the effect of acute hypercapnia on renal total CO2 (tCO2) reabsorption after inhibition of renal carbonic anhydrase. Simultaneous renal clearance studies and free-flow micropuncture studies of the superficial proximal tubule were performed on plasma-repleted Sprague-Dawley rats treated with acetazolamide, 50 mg/kg body weight. Acute hypercapnia (arterial P(CO2), 120 mmHg; blood pH, 7.02) was induced by ventilation with a 10% CO2-90% O2 gas mixture. Control rats (P(CO2), 49.5 mmHg, pH 7.34) were ventilated with room air. The renal fractional excretion of tCO2 was ~20% lower in the hypercapnic group compared with the rats given acetazolamide alone. Acute hypercapnia reduced the fractional delivery of tCO2 to the late proximal tubule by a comparable amount. The absolute proximal reabsorption tCO2 was increased by hypercapnia to 410 ± 47 vs. 170 ± 74 pmol.min-1, P < 0.05. The single nephron glomerular filtration rate was 32.6 ± 0.7 nl.min-1 in the hypercapnic group and 43.8 ± 1.7 nl.min-1 in the rats given acetazolamide only, P < 0.01. Acute hypercapnia enhances renal sympathetic nerve activity. To eliminate this effect, additional experiments were performed in which the experimental kidney was denervated before study. Denervation prevented the change in the single nephron filtration rate during acute hypercapnia, but absolute and fractional proximal tCO2 reabsorption remained elevated in comparison to denervated controls. The concentration of H2CO3 in the late proximal tubule, calculated from the measured luminal pH and bicarbonate concentration and the estimated cortical P(CO2), was higher in the hypercapnic group, which was a finding compatible with H2CO3 cycling from lumen into proximal tubular cell, which provided a source of hydrogen ions for secretion.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 465-473 |
| Number of pages | 9 |
| Journal | Journal of Clinical Investigation |
| Volume | 77 |
| Issue number | 2 |
| State | Published - 1986 |
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Effect of acute hypercapnia on renal and proximal tubular total carbon dioxide reabsorption in the acetazolamide-treated rat. / Winaver, J.; Walker, K. A.; Kunau, R. T.
In: Journal of Clinical Investigation, Vol. 77, No. 2, 1986, p. 465-473.Research output: Contribution to journal › Article
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TY - JOUR
T1 - Effect of acute hypercapnia on renal and proximal tubular total carbon dioxide reabsorption in the acetazolamide-treated rat
AU - Winaver, J.
AU - Walker, K. A.
AU - Kunau, R. T.
PY - 1986
Y1 - 1986
N2 - The present study evaluates the effect of acute hypercapnia on renal total CO2 (tCO2) reabsorption after inhibition of renal carbonic anhydrase. Simultaneous renal clearance studies and free-flow micropuncture studies of the superficial proximal tubule were performed on plasma-repleted Sprague-Dawley rats treated with acetazolamide, 50 mg/kg body weight. Acute hypercapnia (arterial P(CO2), 120 mmHg; blood pH, 7.02) was induced by ventilation with a 10% CO2-90% O2 gas mixture. Control rats (P(CO2), 49.5 mmHg, pH 7.34) were ventilated with room air. The renal fractional excretion of tCO2 was ~20% lower in the hypercapnic group compared with the rats given acetazolamide alone. Acute hypercapnia reduced the fractional delivery of tCO2 to the late proximal tubule by a comparable amount. The absolute proximal reabsorption tCO2 was increased by hypercapnia to 410 ± 47 vs. 170 ± 74 pmol.min-1, P < 0.05. The single nephron glomerular filtration rate was 32.6 ± 0.7 nl.min-1 in the hypercapnic group and 43.8 ± 1.7 nl.min-1 in the rats given acetazolamide only, P < 0.01. Acute hypercapnia enhances renal sympathetic nerve activity. To eliminate this effect, additional experiments were performed in which the experimental kidney was denervated before study. Denervation prevented the change in the single nephron filtration rate during acute hypercapnia, but absolute and fractional proximal tCO2 reabsorption remained elevated in comparison to denervated controls. The concentration of H2CO3 in the late proximal tubule, calculated from the measured luminal pH and bicarbonate concentration and the estimated cortical P(CO2), was higher in the hypercapnic group, which was a finding compatible with H2CO3 cycling from lumen into proximal tubular cell, which provided a source of hydrogen ions for secretion.
AB - The present study evaluates the effect of acute hypercapnia on renal total CO2 (tCO2) reabsorption after inhibition of renal carbonic anhydrase. Simultaneous renal clearance studies and free-flow micropuncture studies of the superficial proximal tubule were performed on plasma-repleted Sprague-Dawley rats treated with acetazolamide, 50 mg/kg body weight. Acute hypercapnia (arterial P(CO2), 120 mmHg; blood pH, 7.02) was induced by ventilation with a 10% CO2-90% O2 gas mixture. Control rats (P(CO2), 49.5 mmHg, pH 7.34) were ventilated with room air. The renal fractional excretion of tCO2 was ~20% lower in the hypercapnic group compared with the rats given acetazolamide alone. Acute hypercapnia reduced the fractional delivery of tCO2 to the late proximal tubule by a comparable amount. The absolute proximal reabsorption tCO2 was increased by hypercapnia to 410 ± 47 vs. 170 ± 74 pmol.min-1, P < 0.05. The single nephron glomerular filtration rate was 32.6 ± 0.7 nl.min-1 in the hypercapnic group and 43.8 ± 1.7 nl.min-1 in the rats given acetazolamide only, P < 0.01. Acute hypercapnia enhances renal sympathetic nerve activity. To eliminate this effect, additional experiments were performed in which the experimental kidney was denervated before study. Denervation prevented the change in the single nephron filtration rate during acute hypercapnia, but absolute and fractional proximal tCO2 reabsorption remained elevated in comparison to denervated controls. The concentration of H2CO3 in the late proximal tubule, calculated from the measured luminal pH and bicarbonate concentration and the estimated cortical P(CO2), was higher in the hypercapnic group, which was a finding compatible with H2CO3 cycling from lumen into proximal tubular cell, which provided a source of hydrogen ions for secretion.
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M3 - Article
C2 - 3080476
AN - SCOPUS:0022553979
VL - 77
SP - 465
EP - 473
JO - Journal of Clinical Investigation
JF - Journal of Clinical Investigation
SN - 0021-9738
IS - 2
ER -