Ullrich K J, Rumrich G, Klöss S
Pflugers Arch. 1978 Oct 18;377(1):33-42. doi: 10.1007/BF00584371.
Inorganic phosphate (Pi) transport was evaluated using the standing droplet method with simultaneous microperfusion of the peritubular capillaries. To evaluate rather small differences in Pi transport and to eliminate the influence of tubular heterogeneity, the technique of crossed paired samples was applied. 1. In chronic PTX rats changing the luminal or both luminal and peritubular pH by varying the HCO-3-concentration between 4 and 50 mmol/l at constant 5% CO2 had no influence on Pi transport. 2. If, however, bicarbonate was omitted from the perfusate and 2 mmol/l phosphate (pH 7.4) was the only buffer, Pi transport was decreased from the control. It was, however, further reduced when the perfusates were gased with 5% CO2 i.e. the starting pH was 5.6. 3. When the solutions contained HEPES buffer (25 mmol/l), Pi transport at pH 8 was much larger than at pH 6.0. 4. Raising the CO2 pressure from 35 to 70 mm Hg did not change the Pi transport when both perfusates had a HCO-3-concentration of 25 mmol/l. It reduced, however, the Pi transport, when the luminal perfusate had only 4 mmol/l bicarbonate. 5. Lowering the CO2 pressure from 38 to 7.6 mm Hg did hardly change the Pi transport when the luminal perfusate contained 4 mmol/l bicarbonate. It lowered, however, the Pi transport significantly when the luminal perfusate had 2k mmol/l bicarbonate. 6. Acetazolamide, 10-4M, lowered the Pi transport when the luminal perfusate contained 4 or 25 mmol/l bicarbonate. At 4 mmol/l luminal HCO-3, raising the pCO2 to 228 mmol/l depressed Pi transport even more. At 25 mmol/l luminal bicarbonate, raising the pCO2 from 38 to 114 mm Hg reversed the acetazolamide inhibition of the Pi transport almost completely. The data indicate that luminal acidosis and intracellular alkalosis inhibits the transtubular Pi transport. A shift of the intracellular pH to a more alkaline value seems to be responsible for the inhibition of Pi transport by acetazolamide, while omission of buffer from the perfusate inhibits Pi transport by effecting an acidic luminal pH.
采用站立液滴法并同时对肾小管周围毛细血管进行微量灌注来评估无机磷酸盐(Pi)转运。为了评估Pi转运中相当小的差异并消除肾小管异质性的影响,应用了交叉配对样本技术。1. 在慢性PTX大鼠中,在5% CO₂恒定的情况下,通过将HCO₃⁻浓度在4至50 mmol/L之间变化来改变管腔或管腔和肾小管周围的pH值,对Pi转运没有影响。2. 然而,如果灌注液中省略碳酸氢盐,且2 mmol/L磷酸盐(pH 7.4)是唯一的缓冲剂,Pi转运较对照组降低。然而,当灌注液用5% CO₂通气即起始pH为5.6时,Pi转运进一步降低。3. 当溶液含有HEPES缓冲剂(25 mmol/L)时,pH 8时的Pi转运远大于pH 6.0时。4. 当两种灌注液的HCO₃⁻浓度均为25 mmol/L时,将CO₂压力从35 mmHg提高到70 mmHg不会改变Pi转运。然而,当管腔灌注液仅含有4 mmol/L碳酸氢盐时,Pi转运降低。5. 当管腔灌注液含有4 mmol/L碳酸氢盐时,将CO₂压力从38 mmHg降低到7.6 mmHg几乎不会改变Pi转运。然而,当管腔灌注液含有20 mmol/L碳酸氢盐时,Pi转运显著降低。6. 10⁻⁴M乙酰唑胺在管腔灌注液含有4或25 mmol/L碳酸氢盐时会降低Pi转运。在管腔HCO₃⁻为4 mmol/L时,将pCO₂提高到228 mmHg会进一步抑制Pi转运。在管腔碳酸氢盐为25 mmol/L时,将pCO₂从38 mmHg提高到114 mmHg几乎完全逆转了乙酰唑胺对Pi转运的抑制作用。数据表明管腔酸中毒和细胞内碱中毒会抑制跨肾小管Pi转运。细胞内pH向更碱性值的转变似乎是乙酰唑胺抑制Pi转运的原因,而灌注液中省略缓冲剂通过影响酸性管腔pH来抑制Pi转运。