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

Abstract

SUMMARY Disorders of calcium metabolism are not generally considered important either clinically or patbophysiologkally 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 arine chemistries in 34 hypertensives. Their mean PTH, 79.1 ± 3.1 filter Eq/ziUter, was rignlflcaatiy higher {p < 0.025) than the mean PTH, 66.9 ± 33, of an age-and sex-matched nonnotenshe control population. The mean serum calcium, 9.5 ± 0.1 mg%, was identical in the two populations. Compared to a second age-aad sex-matched normotensive population, the hypertensives demonstrated a significant (p < 0.005) relatiTe hypercalduria. For any lerd of urinary sodium, hypertenshes excreted more calcium. These preliminary data suggest that parathyroid gland function may be enhanced in essential hypertension. This increased gland actirity appears, in part, to be an appropriate, physiologic response to a previously unrecognized relative hypercalduria, or renal caldum leak, associated with essential hypertension. We condude that the increased prevalence of hypertension in subjects with byperparathyroidfam probably represents the final event In a continuum that begins with obligatory urinary caldum 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 patbogenesis of human and experimental hypertension. 1 "' Conversely, the prevalence of hyperparathyroidism may be two to eight times greater in hypertensive than in normotensive subjects. 4-• In addition, thiazide diuretics cause overt hypercalcemia in certain hyper-

Trabecular bone area and bone healing in spontaneously hypertensive rats: a histometric study

“…Angiotensin II is the major mediator of the maintenance of extracellular fluid volume and blood pressure and may decelerate osteoblastic differentiation and bone formation and activate osteoclasts and bone resorption. [4][5][6][7][21][22][23] Although some studies have already reported the influence of hypertension on bone density, the results of the present study contribute to the original information regarding the negative effect of hypertension on the early stages of bone healing in a surgicallycreated critical-size defect. A mechanism that could partially explain our histometric results may also be attributed to the influence of angiotensin II on bone cells.…”

“…2,3 Essential hypertension may be linked to the increased mobilization of calcium from bone, to the increased losses of calcium from kidney, to the secondary activation of the parathyroid hormone (PTH) and to the angiotensin II activating bone cells. [4][5][6][7] Bone healing is composed of a series of overlapping stages involving the coordinated action of several cell lineages on a cascade of biological events, and has always been one of the most important concerns in medicine and dentistry. The use of some drugs (i.e.…”

Prevention of osteoporosis by angiotensin-converting enzyme inhibitor in spontaneous hypertensive rats

“…Compared with healthy controls, reduced bone mineral density (BMD) has been found in patients with hypertension or ischemic heart disease. [1][2][3][4] Clinical studies have shown significant abnormalities in calcium metabolism in hypertension, [5][6][7] and a decreased circulating level of calcium results in an increased parathyroid hormone, which is implicated in the occurrence and/or development of hypertension. 8 Animal and epidemiological evidence suggests that high blood pressure is associated with abnormalities of calcium metabolism, leading to an increase in calcium loss, to a secondary activation of the parathyroid gland and to an increased movement of calcium from bone, thereby increasing the risk of osteoporosis.…”

Effectiveness of 1,25-dihydroxyvitamin D Supplementation on Blood Pressure Reduction in a Pseudohypoparathyroidism Patient with High Renin Activity.

“…The relationship between hypertension and serum PTHand calcium levels suggests that a high PTHlevel may cause hypertension in PsHP. The association between blood pressure and PTHis well known in normotensives (3,4), hypertensives (5)(6)(7)(8), and old aged persons (9). Although vitamin D therapy can ameliorate the elevated serum PTHlevel in PsHP (10), there are no reports whether such supplementation is also effective in reducing blood pressure in PsHP.…”