AJP - Renal Physiology, Vol 242, Issue 5 447-F452, Copyright © 1982 by American Physiological Society
Nicotinamide restores phosphaturic effect of PTH and calcitonin in phosphate deprivation
T. J. Berndt, J. D. Pfeifer, F. G. Knox, S. A. Kempson and T. P. Dousa
Results of previous studies suggest a potentially important role for
nicotinamide adenine dinucleotide (NAD) in the cellular regulation of
phosphate transport by the renal proximal tubules. The present clearance
studies were performed to evaluate whether intraperitoneal administration
of nicotinamide, a precursor of NAD and inhibitor of NAD catabolism, would
not only increase phosphate excretion but also restore the phosphaturic
response to parathyroid hormone (PTH) in rats fed a low phosphate diet.
Rats fed a low phosphate diet were resistant to the phosphaturic effect of
PTH, calcitonin, and dibutyryl cAMP (DBcAMP) in spite of the fact that all
three agents elicited an increase in the urinary excretion of cAMP.
Administration of nicotinamide to rats fed a low phosphate diet increased
renal cortical NAD levels, increased phosphate excretion, partially
restored the phosphaturic effect of PTH and DBcAMP, and completely restored
the phosphaturic response to calcitonin. We conclude that nicotinamide
restores the phosphaturic effect of PTH and calcitonin in rats fed a low
phosphate diet by acting at a cellular step subsequent to cAMP generation
to inhibit tubular reabsorption of phosphate.
