Enhanced parathyroid function in essential hypertension: a homeostatic response to a urinary calcium leak.

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.