Plasma bicarbonate decreases during normal pregnancy. To assess what roles increased extra cellular volume or alterations in parathyroid hormone levels (iPTH) have in the maintenance of this decrement, we evaluated acid-base metabolism in eleven 3rd-trimester women. Base-line pH and PCO2 were 7.44 and 27.3 mmHg, respectively. Mean tubular reabsorption of phosphate was 93% and baseline iPTH levels were similar to those of nonpregnant subjects. During the slow infusion of hypertonic NaHCO3, a urinary threshold of HCO3- (THCO3) appeared at a mean plasma level of 18.9 meq/liter, but as plasma HCO3- increased progressively, its renal reclamation was almost complete and there was no evidence of either splay or tubular maximum, even when filtered loads of HCO3- reached 5 meq/min. Urine acidification was normal and distal [H+] secretory ability( deltaidification was normal and distal [H+] secretory ability (delta urinary PCO2) was similar to that reported in nongravid subjects. In metabolic balance studies blood pH and plasma HCO3- increased (P less than .01 and less than .02, respectively) when the women changed from a high- to a low-sodium diet. Mechanisms by which decreased plasma bicarbonate levels are maintained during gestation are discussed.
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Renal function was measure before and shortly after uninephrectomy in mice to evaluate if work expended in the reabsorption of glomerular filtrate plays a role in the initiation of compensatory growth. To exclude the possibility of small but undetectable increments in glomerular filtration rate and absolute sodium reabsorption these functions were experimentally reduced immediately after uninephrectomy and sham nephrectomy. The onset of growth was indicated by an increased rate of [14C]choline incorporation into phospholipid in renal cortical slices. [14C]choline incorporation increased significantly only after uninephrectomy and remained unchanged after sham operation regardless of the magnitude or direction of the concurrent change in sodium reabsorption. The rate of incorporation increased by 40 +/- 8% (P less than 0.005) in uninephrectomized animals whose sodium reabsorption was reduced by 34 +/- 6% (P less than 0.001) and rose 45 +/- 11% (P less than 0.005) when sodium reabsorption remained unchanged. These results indicate that compensatory kidney growth is not triggered by an increase in renal work expended in the reabsorption of glomerular filtrate; in fact, it can occur when reabsorptive work is substantially decreased.
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