Advertisement

Free access | 10.1172/JCI107632

The Acute Effect of 25-Hydroxycholecalciferol on Renal Handling of Phosphorus: EVIDENCE FOR A PARATHYROID HORMONE-DEPENDENT MECHANISM

Mordecai M. Popovtzer, John B. Robinette, Hector F. Deluca, and Michael F. Holick

Department of Medicine, University of Colorado School of Medicine, Denver, Colorado 80220

Veterans Administration Hospital, Denver, Colorado 80220

Department of Biochemistry, University of Wisconsin, Madison, Wisconsin 53706

Find articles by Popovtzer, M. in: JCI | PubMed | Google Scholar

Department of Medicine, University of Colorado School of Medicine, Denver, Colorado 80220

Veterans Administration Hospital, Denver, Colorado 80220

Department of Biochemistry, University of Wisconsin, Madison, Wisconsin 53706

Find articles by Robinette, J. in: JCI | PubMed | Google Scholar

Department of Medicine, University of Colorado School of Medicine, Denver, Colorado 80220

Veterans Administration Hospital, Denver, Colorado 80220

Department of Biochemistry, University of Wisconsin, Madison, Wisconsin 53706

Find articles by Deluca, H. in: JCI | PubMed | Google Scholar

Department of Medicine, University of Colorado School of Medicine, Denver, Colorado 80220

Veterans Administration Hospital, Denver, Colorado 80220

Department of Biochemistry, University of Wisconsin, Madison, Wisconsin 53706

Find articles by Holick, M. in: JCI | PubMed | Google Scholar

Published March 1, 1974 - More info

Published in Volume 53, Issue 3 on March 1, 1974
J Clin Invest. 1974;53(3):913–921. https://doi.org/10.1172/JCI107632.
© 1974 The American Society for Clinical Investigation
Published March 1, 1974 - Version history
View PDF
Abstract

The acute effect of i.v. and direct intrarenal arterial infusion of 25-hydroxycholecalciferol (25HCC) and 1,25-dihydroxycholecalciferol (1,25-DHCC) on renal handling of phosphorus was evaluated in the following groups of rats: (a) intact animals, (b) parathyroidectomized (PTX) hypocalcemic rats, (c) PTX rats in which normocalcemia was maintained with calcium supplements and (d) PTX animals in which urinary phosphorus was augmented by (i) i.v. sodium phosphate, (ii) expansion of the extracellular fluid volume with normal saline, and (iii) i.v. parathyroid hormone (PTH). Clearances of inulin (CIn), phosphorus (CP), and fractional clearances of phosphorus (CP/CIn) of the experimental groups were compared with those of the corresponding control groups, and the clearances of the infused kidneys with those of the contralateral kidneys.

In intact animals, i.v. 25HCC decreased CP/CIn from 0.29±0.04 (mean ±SE) to 0.19±0.04, and i.v. 1,25-DHCC decreased CP/CIn from 0.25±0.04 to 0.15±0.02. The intrarenal infusion of both 25HCC and 1,25DHCC into intact animals failed to produce a unilateral change; however, it decreased CP/CIn bilaterally. i.v. and intrarenal infusions of 25HCC or 1,25DHCC in PTX hypocalcemic and normocalcemic rats, and i.v. infusions of 25HCC in PTX rats receiving either sodium phosphate or normal saline, all failed to produce significant changes in CP/CIn. In contrast, 24HCC given i.v. to PTX animals receiving exogenous PTH was associated with a significant fall in CP/CIn, from 0.34±0.08 to 0.13±0.02. These results indicate that 25HCC enhances tubular reabsorption of phosphorus in rats, only in the presence of either endogenous or exogenous circulating PTH, but not in its absence and thus imply a PTH-dependent mechanism of 25HCC action on the kidney. This effect does not appear to be related to the conversion of 25HCC into 1,25DHCC, since the latter fails to affect tubular reabsorption of phosphorus in PTX rats.

Browse pages

Click on an image below to see the page. View PDF of the complete article

Version history
  • Version 1 (March 1, 1974): No description
Advertisement
Advertisement