AJP - Renal Physiology, Vol 253, Issue 4 726-F733, Copyright © 1987 by American Physiological Society
Hypocalcemia-associated modulation of renal response to acute volume expansion in rats
D. E. Wesson
Department of Medicine, Veterans Administration Medical Center, Houston, Texas 77211.
The present study used free-flow micropuncture and whole-kidney clearance
studies to determine the renal response to normocalcemic vs. hypocalcemic
acute volume expansion (AVE) in anesthetized Munich-Wistar rats. Animals
received AVE with Ringer bicarbonate to 10% body weight; half of these
animals were supplemented with calcium to maintain normocalcemia (VE +
Ca2+) and half were allowed to become hypocalcemic (VE). Filtered load of
chloride and total CO2 (TCO2) to the superficial proximal tubule and
delivered load to the superficial loop segment were not different between
groups. Superficial proximal tubule absolute Cl reabsorption was not
different, but superficial loop segment absolute Cl reabsorption was less
in the VE + Ca2+ animals (2,221 +/- 106 vs. 2,651 +/- 125 pmol/min, P less
than 0.05) and whole-kidney fractional chloride excretion was greater (10.5
+/- 1.6 vs. 4.3 +/- 0.5%, P less than 0.05). When indomethacin (I) was
administered to hypocalcemic (VE + I) and normocalcemic (VE + Ca2+ + I) AVE
animals, both groups of animals had tubular and whole-kidney chloride
reabsorption similar to VE animals. TCO2 reabsorption was not influenced by
Ca2+ or I. The data indicate that normocalcemic vs. hypocalcemic AVE
results in reduced superficial loop segment chloride reabsorption and
greater whole-kidney fractional chloride excretion in the absence but not
in the presence of prostaglandin inhibition. The data are compatible with
an effect of hypocalcemia during AVE to limit superficial loop segment and
whole-kidney chloride excretion by inhibiting renal prostaglandin
synthesis.
