AJP - Renal Physiology, Vol 256, Issue 1 29-F34, Copyright © 1989 by American Physiological Society
Bicarbonate reabsorption by the kidney of the newborn rabbit
A. J. van der Heijden and J. P. Guignard
Department of Pediatrics, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland.
Bicarbonate reabsorption by the immature kidney in response to acute
acid-base changes was assessed in 50 anesthetized newborn rabbits before
the end of nephrogenesis. The normal newborn rabbit (age 5-12 days) is in a
state of hypochloremic metabolic alkalosis (PHCO3-, 31.9 +/- 0.6 mmol/l;
PCl-, 83.1 +/- 1.0) and excretes a hypertonic (Uosmol = 578 +/- 41
mosmol/kgH2O), alkaline (UpH = 7.40 +/- 0.15) urine containing 50 +/- 9
mmol/l Cl- and 13 +/- 4 mmol/l Na+. The alkalosis is probably generated by
an alkaline load contained in the mother's milk and maintained by a state
of chloride wasting and volume contraction. In this alkalotic model,
bicarbonate reabsorption, expressed per milliliter glomerular filtration
rate (GFR), correlates positively with arterial CO2 pressure (PaCO2). The
ability of the immature kidney to reclaim filtered bicarbonate in response
to an elevation of the plasma carbon dioxide tension remains unlimited up
to PaCO2 of 110 mmHg (y = 20.7 + 0.15 x, r = 0.82, P less than 0.001).
Hypercapnia is associated with a marked fall in GFR, so that the positive
correlation between bicarbonate reabsorption and PaCO2 vanishes when the
bicarbonate reabsorption rate is expressed in absolute terms. Bicarbonate
reabsorption is strongly dependent on the filtered load during both acutely
induced metabolic acidosis and alkalosis. The acid-base state of the
newborn rabbit is in sharp contrast with that of most animal species, and
the renal handling of bicarbonate as a function of GFR does not show signs
of tubular immaturity.
