Hypertension, Vol 2, 162-168, Copyright © 1980 by American Heart Association
DA McCarron, PA Pingree, RJ Rubin, SM Gaucher, M Molitch and S Krutzik
Disorders of calcium metabolism are not generally considered important
either clinically or pathophysiologically in essential hypertension. Recent
reports, though, suggest that increased parathyroid gland function may be
one of the more common endocrine disturbances associated with hypertension.
We measured serum parathyroid hormone (PTH) concentrations as well as
routine blood and urine chemistries in 34 hypertensives. Their mean PTH,
79.1 +/- 3.1 muliter Eq/muliter, was significantly higher (p less than
0.025) than the mean PTH, 66.9 +/- 3.3, of an age- and sex-matched
normotensive control population. The mean serum calcium, 9.5 +/- 0.1 mg%,
was identical in the two populations. Compared to a second age- and
sex-matched normotensive population, the hypertensives demonstrated a
significant (p less than 0.005) relative hypercalciuria. For any level of
urinary sodium, hypertensives excreted more calcium. These preliminary data
suggest that parathyroid gland function may be enhanced in essential
hypertension. This increased gland activity appears, in part, to be an
appropriate, physiologic response to a previously unrecognized relative
hypercalciuria, or renal calcium leak, associated with essential
hypertension. We conclude that the increased prevalence of hypertension in
subjects with hyperparathyroidism probably represents the final event in a
continuum that begins with obligatory urinary calcium losses in
hypertensives, but whose pathological presentation is hyperparathyroidism.
The results of this pilot study indicate a need for derivative experiments
directed at defining the importance of our preliminary findings in the
pathogenesis of human and experimental hypertension.
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Enhanced parathyroid function in essential hypertension: a homeostatic response to a urinary calcium leak
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