Langberg H, Hartmann A, Kiil F
Kidney Int. 1984 Aug;26(2):128-36. doi: 10.1038/ki.1984.146.
Glomerular filtration rate (GFR) was altered by varying renal perfusion pressure in volume-expanded, anesthetized dogs infused with ethacrynic acid. Phosphate reabsorption varied linearly with GFR (r greater than 0.9), 0.83 of the increase in filtered load being reabsorbed. Phosphate reabsorption at comparable filtered loads was not significantly changed by raising plasma bicarbonate concentration from 30 to 55 mM and adjusting PCO2 to keep plasma pH constant. Plasma pH was altered by inducing hyper- and hypocapnia or infusing bicarbonate. Plasma phosphate concentration varied with plasma pH before phosphate infusion and was kept constant at 3.4 +/- 0.1 mM in intact and thyroparathyroidectomized dogs; some of which were also examined during hyperchloremic acidosis. At comparable GFR, phosphate and bicarbonate reabsorption correlated (r greater than 0.9), except during acidosis when the filtered load of bicarbonate became inadequate. In all experiments phosphate reabsorption and plasma pH correlated (r greater than 0.85). Compared with control values at plasma pH 7.4, phosphate reabsorption increased by about 40% during acidosis (pH 7.1) and decreased by about 50% during alkalosis (pH 7.8) both in intact and thyroparathyroidectomized dogs. We propose that net hydrogen ion secretion is the common determinant of phosphate and bicarbonate reabsorption.
在输注依他尼酸的容量扩张麻醉犬中,通过改变肾灌注压来改变肾小球滤过率(GFR)。磷酸盐重吸收与GFR呈线性变化(r大于0.9),滤过负荷增加量的0.83被重吸收。将血浆碳酸氢盐浓度从30 mM提高到55 mM并调节PCO₂以保持血浆pH恒定,在相当的滤过负荷下磷酸盐重吸收无显著变化。通过诱导高碳酸血症和低碳酸血症或输注碳酸氢盐来改变血浆pH。在输注磷酸盐之前,血浆磷酸盐浓度随血浆pH变化,在完整和甲状旁腺切除的犬中保持在3.4±0.1 mM恒定;其中一些犬在高氯性酸中毒期间也进行了检查。在相当的GFR下,磷酸盐和碳酸氢盐重吸收相关(r大于0.9),但在酸中毒期间,当碳酸氢盐滤过负荷不足时除外。在所有实验中,磷酸盐重吸收与血浆pH相关(r大于0.85)。与血浆pH 7.4时的对照值相比,在完整和甲状旁腺切除的犬中,酸中毒(pH 7.1)期间磷酸盐重吸收增加约40%,碱中毒(pH 7.8)期间减少约50%。我们提出,净氢离子分泌是磷酸盐和碳酸氢盐重吸收的共同决定因素。