AJP - Regulatory, Integrative and Comparative Physiology, Vol 258, Issue 1 120-R123, Copyright © 1990 by American Physiological Society
Propranolol restores phosphaturic effect of PTH in short-term phosphate deprivation
A. Rybczynska, A. Hoppe and F. G. Knox
Department of Physiology, Mayo Clinic and Foundation, Rochester, Minnesota 55905.
Phosphate deprivation causes a resistance to the phosphaturic effect of
parathyroid hormone (PTH). The present study evaluated the role of the
beta-adrenergic system in this resistance phenomenon. In clearance
experiments performed on acutely thyroparathyroidectomized male
Sprague-Dawley rats, the phosphaturic response to PTH was determined in the
presence and absence of propranolol in rats fed a low-phosphate diet (LPD)
for 0.5, 1, 2, 3, or 4 days. Fractional excretion of phosphate (FEPi) in
control rats fed a normal-phosphate diet (NPD) increased from 4.37 +/- 1.6
to 38.5 +/- 3.4% in response to PTH infusion. Propranolol did not change
FEPi in NPD animals in the absence or in the presence of PTH (2.0 +/- 1.1
vs. 36.7 +/- 1.6%). LPD resulted in a gradual decrease in the phosphaturic
response to PTH infusion as compared with NPD animals. PTH increased FEPi
to 24.2 +/- 6.0% after one-half day of LPD, but when the infusion was
supplemented with propranolol, PTH increased FEPi to 38.0 +/- 4.7%, similar
to that in NPD animals. In the group fed LPD for one day, PTH increased
FEPi to 16.9 +/- 4.3%, whereas in the presence of propranolol FEPi was
restored to a similar level as in the NPD group (36.0 +/- 5.9%). Two days
of LPD markedly decreased FEPi in response to PTH to 7.9 +/- 3.8% as
compared with NPD rats, and propranolol infusion did not change this value
significantly. Three and 4 days of LPD induced complete resistance to the
phosphaturic effect of PTH in the presence as well as in the absence of
propranolol.(ABSTRACT TRUNCATED AT 250 WORDS)
