Parathyroid hormone-related protein and arteriolar tone in hypertensives

Abstract

Parathyroid hormone-related protein (PTHrP) is involved in the hypercalcemia of malignancy and expressed by a number of tumours. It is also produced by normal tissues (such heart, brain, kidney, and vascular smooth cells). It has been demonstrated that PTHrP like parathyroid hormone (PTH) induces vasodilation and positive chronotropic and inotropic action in the rat, and an involvement of the adrenergic and RAA system has been postulated. Therefore, the aim of the study was to evaluate serum middle molecular immunoreactive PTH (iPTH-MM), intact [1–84] iPTH, iPTHrP levels and PRA in supine and standing position, and daily urinary catecholamine (Ur.Tot.CAT) excretion in 17 essential hypertensive patients and in 15 sex- and age-matched normotensive control subjects.

Serum iPTH-MM, intact iPTH, and iPTHrP levels were significantly higher in hypertensives than in N subjects. Orthostatic stimulus significantly increased iPTH-MM and intact iPTH levels in both groups, while no change in serum iPTHrP was observed. Finally, in hypertensives a positive correlation was found between orthostatic change of intact [1-84] iPTH levels, Ur.Tot.CAT excretion, and PRA, but not between orthostatic change of iPTHrP, Ur.Tot.CAT excretion, and PRA.

These results confirm a close link between glandular PTH secretion and adrenergic and RAA system. Since an influence of the adrenergic and RAA system on PTHrP secretion seems to fail, a tissue but not glandular source of PTHrP could be suggested. Particularly, the high serum iPTHrP levels observed in hypertensives could arise locally from the cardiovascular system (heart and vascular smooth muscle cells) as a vasodilative homeostatic response to the arteriolar hypertone and vascular damage induced by hypertension.