Cardiovascular effects of human parathyroid hormone and parathyroid hormone-related peptide

Parathyroid hormone (PTH) is hypotensive in mammals and is a potent coronary vasodilator. Parathyroid hormone-related peptide (PTHrp) has been reported to have similar vascular activity. In the present study, the effects of human PTH (hPTH) and human PTHrp (hPTHrp) were compared in various in vivo and in vitro assays. In vivo studies included blood pressure measurement and coronary blood flow determination with labeled microspheres in anesthetized and cannulated normotensive rats. Isolated rat tail artery and portal vein helical strips were used in studying tension development in vitro. In the blood pressure assay, PTHrp was several times more potent than PTH. PTHrp was also significantly more potent than PTH in relaxing tail artery precontracted with arginine vasopressin (AVP). PTHrp and PTH both inhibited the spontaneously contracting portal vein, but again PTHrp was significantly more potent. PTHrp (1 microgram/kg) produced a greater increase in coronary blood flow as compared with the same dose of PTH. These data suggest that PTHrp is more potent than PTH in its cardiovascular actions. It is possible that PTHrp is the endogenous vasodilating ligand, and the structural similarity between PTH and PTHrp may explain the pharmacological action of PTH. It is therefore unlikely that PTH or PTHrp may be involved in the genesis or maintenance of hypertension. Because the parathyroid gland seems to be involved in some forms of essential hypertension, factor(s) other than PTH or PTHrp may be responsible.