Cogan M G
Science. 1985 Sep 27;229(4720):1405-7. doi: 10.1126/science.2930899.
The kidney maintains the elevated plasma concentration of bicarbonate that occurs in chronic metabolic alkalosis. A reduction in the glomerular filtration rate (GFR) can maintain the filtered bicarbonate load at a normal level so that a normal rate of bicarbonate reabsorption suffices to prevent urinary excretion of this anion. It is also possible that bicarbonate reabsorption might increase so as to maintain the alkalosis if GFR were not reduced. To examine this latter possibility, atrial natriuretic factor was used in alkalotic rats to restore a more normal GFR and to increase the amount of bicarbonate filtered by the glomerulus. Proximal bicarbonate reabsorption remained relatively static. Higher than normal amounts of bicarbonate were then delivered out of the proximal tubule, bicarbonate appeared in the urine, and the plasma concentration of bicarbonate fell. A reduction in GFR is thus necessary for the maintenance of chronic metabolic alkalosis. Normalizing GFR induces bicarbonaturia and initiates repair of the alkalosis.
肾脏维持慢性代谢性碱中毒时出现的血浆碳酸氢盐浓度升高。肾小球滤过率（GFR）降低可使滤过的碳酸氢盐负荷维持在正常水平，从而使正常的碳酸氢盐重吸收率足以防止该阴离子从尿液中排泄。如果GFR不降低，碳酸氢盐重吸收也有可能增加以维持碱中毒。为了研究后一种可能性，在碱中毒大鼠中使用心房利钠因子来恢复更正常的GFR，并增加肾小球滤过的碳酸氢盐量。近端碳酸氢盐重吸收保持相对稳定。然后，高于正常量的碳酸氢盐从近端小管排出，尿液中出现碳酸氢盐，血浆碳酸氢盐浓度下降。因此，GFR降低对于维持慢性代谢性碱中毒是必要的。使GFR正常化会导致尿中出现碳酸氢盐，并启动碱中毒的纠正。
