AJP - Renal Physiology, Vol 249, Issue 3 361-F365, Copyright © 1985 by American Physiological Society
Response of serum 1,25(OH)2D3 to variation of ionized calcium during chronic acidosis
D. A. Bushinsky, G. S. Riera, M. J. Favus and F. L. Coe
Chronic ammonium chloride (NH4Cl) administration causes metabolic acidosis
and prevents the normal rise of serum 1,25-dihydroxyvitamin D3
[1,25(OH)2D3] during a low-calcium diet (LCD, 0.002% calcium). The
suppression of serum 1,25(OH)2D3 was not due to reduced parathyroid hormone
concentration, elevated serum phosphorus, or total calcium concentration.
Acidosis increased blood ionized Ca [Ca2+] and proton [H+] concentrations.
Serum 1,25(OH)2D3 levels were inversely correlated with both [Ca2+] and
[H+]. To determine the independent effects of [Ca2+] on serum 1,25(OH)2D3
we varied [Ca2+] at a constant [H+] by infusing either EGTA or saline for
24 h after 11 days of LCD and NH4Cl. EGTA, preequilibrated with three
concentrations of Ca, lowered [Ca2+] and raised 1,25(OH)2D3 but did not
alter [H+] or serum phosphorus concentration. The log of serum 1,25(OH)2D3
varied linearly and inversely with arterial blood [Ca2+] during saline (r =
-0.884, n = 8, P less than 0.001) and EGTA infusions (r = -0.798, n = 22, P
less than 0.001). At all levels of [Ca2+], rats infused with EGTA had a
higher serum 1,25(OH)2D3 than those infused with saline. Log serum
1,25(OH)2D3 was correlated neither with [H+] nor pH. Elevated [Ca2+] and
not [H+] appears to suppress the serum 1,25(OH)2D3 response to LCD during
NH4Cl acidosis in the rat.
