AJP - Renal Physiology, Vol 253, Issue 1 34-F40, Copyright © 1987 by American Physiological Society
Effect of acute hypercapnia on PTH-stimulated phosphaturia in dietary Pi-deprived rat
J. Guntupalli, B. Matthews, B. Carlin and E. Bourke
The effects of respiratory acidosis on renal inorganic phosphate (Pi)
handling are controversial. Clearance experiments, therefore, were
performed in fasted, chronically parathyroidectomized (PTX), dietary
Pi-deprived rats. The objectives were twofold: to study the effects of
compensated and uncompensated hypercapnia per se on renal Pi excretion and
to examine the interaction between acute hypercapnia, dietary Pi, and
parathyroid hormone (PTH) on the renal handling of Pi. Acute hypercapnia
increased the plasma Pi (delta 2.82 +/- 0.65 mg/dl, P less than 0.05)
without altering the glomerular filtration rate (GFR). The FEPi increased
(delta 7.26 +/- 0.48%, P less than 0.001) but the TRPi/GFR also increased.
PTH (3 U X kg-1 X h-1) superimposed on hypercapnia resulted in a plasma Pi
comparable to hypercapnia alone. The FEPi (7.56 +/- 0.78 vs. 24.43 +/-
2.20%; P less than 0.001) was higher and the TRPi/GFR (117 +/- 4 vs. 80 +/-
2 micrograms/min, P less than 0.01) lower, in the former group. PTH
infusion during normocapnia resulted in a lower FEPi (0.20 +/- 0.10 vs.
24.43 +/- 2.20%, P less than 0.001) and a higher TRPi/GFR (106 +/- 2 vs. 80
+/- 2 micrograms/min, P less than 0.01) compared with PTH infusion during
hypercapnia. Urinary adenosine 3',5'-cyclic monophosphate (cAMP) excretion
was similar between the groups. During hypercapnia, when the extracellular
acidemia was neutralized, the phosphaturic action of PTH persisted. These
studies offer direct evidence that in chronically PTX, dietary Pi-deprived
rats, the phosphaturic action of PTH is restored by hypercapnia per se.
This effect appears to be independent of extracellular acidemia, changes in
the plasma Pi and calcium, urinary pH and Na and cAMP excretion.
