This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Merke, J. Articles by Ritz, E. Search for Related Content PubMed PubMed Citation Articles by Merke, J. Articles by Ritz, E.

Hypertension, Vol 13, 233-242, Copyright © 1989 by American Heart Association

ARTICLES

Hyperparathyroidism and abnormal calcitriol metabolism in the spontaneously hypertensive rat

J Merke, PA Lucas, A Szabo, G Cournot-Witmer, G Mall, R Bouillon, T Drueke, J Mann and E Ritz
Department of Internal Medicine, University of Heidelberg, Federal Republic of Germany.

Abnormalities of calcium metabolism and of its two principal regulating hormones, parathyroid hormone and 1,25-dihydroxyvitamin D3 (calcitriol), have been reported in the spontaneously hypertensive rat (SHR). Reports of abnormal calcitriol metabolism in the SHR by several groups have not provided measurements of tissue calcitriol receptors. Similarly, few data are available as to the parathyroid status of the SHR. In the present study, circulating calcitriol levels and intestinal and parathyroid gland calcitriol receptor status were determined in male SHR and in Wistar-Kyoto (WKY) rats. Parathyroid status was investigated by determination of parathyroid gland mass together with tissue micromorphometry and by quantitative histology of bone as a measure of the biological action of parathyroid hormone. Circulating calcitriol levels were reduced in the 11-week-old SHR compared with the WKY rat (165 +/- 23 vs. 194 +/- 28 pmol/l, p less than 0.01, mean +/- SD). Calcitriol-free ratio was diminished and maximal specific binding capacity for calcitriol was increased in the SHR in parathyroid tissue (172 +/- 4.9 vs. 123 +/- 6.6 fmol/mg protein, p less than 0.01) and in intestinal mucosa with no change of receptor affinity. Plasma ionized calcium (1.29 +/- 0.05 vs. 1.45 +/- 0.35 mmol/l, p less than 0.05) and phosphate (1.5 +/- 0.26 vs. 2.4 +/- 0.03 mmol/l, p less than 0.05) were significantly lower in the SHR. Parathyroid gland mass was increased in the SHR (59 +/- 12 vs. 17 +/- 7 micrograms/100 g body wt, p less than 0.001) as a result of hyperplasia and not hypertrophy. Higher osteoclast numbers were observed in SHR bone (27.6 +/- 0.79 vs. 23.9 +/- 0.66 osteoclasts/mm2, p less than 0.01), suggesting increased parathyroid hormone activity. In summary, in the 11-week-old SHR we observed reduced circulating calcitriol levels together with increased tissue calcitriol receptor numbers, increased parathyroid gland mass, and histological evidence of hyperparathyroidism. It is possible that these abnormalities influence the development of hypertension in the SHR.

This article has been cited by other articles:

				K. E. Armour, K. J. Armour, M. E. Gallagher, A. Godecke, M. H. Helfrich, D. M. Reid, and S. H. Ralston Defective Bone Formation and Anabolic Response to Exogenous Estrogen in Mice with Targeted Disruption of Endothelial Nitric Oxide Synthase Endocrinology, February 1, 2001; 142(2): 760 - 766. [Abstract] [Full Text] [PDF]

				E. Kristal-Boneh, P. Froom, G. Harari, and J. Ribak Association of Calcitriol and Blood Pressure in Normotensive Men Hypertension, November 1, 1997; 30(5): 1289 - 1294. [Abstract] [Full Text]