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Role of Thyroid Hormone in Regulation of Renal Phosphate Transport in Young and Aged Rats¹

Departments of Physiology (A.I.A.), Anatomy (M.S., D.D.), Toxicology (R.M., V.S.), and Pharmacology (J.A.), University of Zaragoza, 50013 Zaragoza, Spain; Institute of Physiology (J.B., H.M.), University of Zürich-Irchel, CH-8057 Zürich, Switzerland; and Department of Internal Medicine (M.L.), University of Texas Southwestern Medical Center and Department of Veterans Affairs Medical Center, Dallas, Texas 75216

Address all correspondence and requests for reprints to: Víctor Sorribas, Ph.D., Departamento de Toxicología, Facultad de Veterinaria, Universidad de Zaragoza, Calle Miguel Servet, 177, E-50013 Zaragoza, Spain. E-mail: sorribas{at}posta.unizar.es

In the present study, we have examined the cellular mechanisms mediating the regulation of renal proximal tubular sodium-coupled inorganic phosphate (Na/P_i) transport by thyroid hormone (T₃) in young and aged rats. Young hypothyroid rats showed a marked decrease in Na/P_i cotransport activity, which was associated with parallel decreases in type II Na/P_i cotransporter (NaPi-2) protein and messenger RNA (mRNA) abundance. In contrast, administration of long-term physiological and supraphysiological doses of T₃ resulted in significant increases in Na/P_i cotransport activity, protein, and mRNA levels. Nuclear run-on experiments indicated that thyroid hormone regulates NaPi-2 mRNA levels by a transcriptional mechanism. In aged rats, although there were no changes in T₃ serum levels (when compared with young animals), there were significant decreases in serum P_i concentration, renal Na/P_i cotransport activity, and NaPi-2 protein and mRNA abundance. These effects were mediated, at least in part, by a reduction in the transcriptional rate of the NaPi-2 gene, probably caused by, among other factors, a smaller response to the stimulatory action of T₃. Compared with young rats, the old rats exhibited less sensitivity of the Na/P_i cotransporter to thyroid hormone, with decreased effects in both hypothyroid (inhibitory) and hyperthyroid (stimulatory) animals.

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