AJP - Renal Physiology, Vol 249, Issue 6 919-F922, Copyright © 1985 by American Physiological Society
Nephron site of resistance to phosphaturic effect of PTH during respiratory alkalosis
T. J. Berndt and F. G. Knox
This study was performed to evaluate the nephron site(s) responsible for
the blunted phosphaturic effect of parathyroid hormone during respiratory
alkalosis. In normocapnic thyroparathyroidectomized rats, parathyroid
hormone administration markedly increased the fractional excretion of
phosphate (FEp) from 2.1 +/- 0.5 to 36.6 +/- 5.0%. However, in the
respiratory alkalotic rats, parathyroid hormone administration did not
significantly increase the FEp (1.4 +/- 0.9 to 5.9 +/- 2.2%). This blunted
phosphaturic response to parathyroid hormone was not due to a blunted
inhibition of phosphate reabsorption by the superficial proximal tubule,
since parathyroid hormone administration significantly increased the
fractional delivery of phosphate (FDp) at the superficial late proximal
tubule in both normal (25.3 +/- 3.0 to 36.2 +/- 3.8%, delta 10.9 +/- 3.2%)
and respiratory alkalotic rats (12.2 +/- 3.1 to 30.3 +/- 4.9%, delta 18.0
+/- 4.7%). Parathyroid hormone administration significantly increased the
FDp at the superficial early distal tubule from 9.3 +/- 3.9 to 38.7 +/-
7.4% (delta 29.4 +/- 5.1%) in normal rats and from 4.5 +/- 1.7 to 12.9 +/-
3.4% (delta 8.5 +/- 3.2%) in the respiratory alkalotic rats. We conclude
that the blunted phosphaturic response to parathyroid hormone in
respiratory alkalotic rats is not due to a blunted inhibition of phosphate
reabsorption by the proximal convoluted tubule but is primarily due to
enhanced reabsorption by the pars recta segment of the proximal tubule.
