The vascular actions of parathyroid hormone (PTH) are not well understood. In human studies there is a remarkable incidence of hypertension (20-50%) in patients with hyperparathyroidism. Also about 1 in 130 hypertensive patients is likely to have primary hyperparathyroidism. Hyperparathyroidism, as the name implies, is characterized by markedly elevated serum PTH levels and hypercalcemia. Despite this well documented link between hypertension and hyperparathyroidism recent studies have shown that PTH is a potent vasodilator substance in dogs, rabbits and rats. The purpose of the present study is to more closely examine this apparent paradox between the vasodilator effects of PTH and its association with hypertension. The vascular actions of PTH will be studied at various levels of organization in an attempt to determine the direct and indirect effects of PTH on vascular tone. As our preliminary evidence indicates, PTH causes an increase in cyclic AMP in rat vascular smooth muscle (VSM) cells grown in culture. PTH also stimulates adenylate cyclase activity in membranes prepared from VSM cells. Rat aortic strips undergo a rapid and dose-dependent relaxation after PTH treatment. Further biochemical characterization of the effects of PTH on VSM cells and vascular tissue is needed including measurement and characterization of PTH receptors. The importance of endothelial-derived vasodilator substances in the hypotensive action of PTH will be evaluated in rat aortic strips with the intimal layer rubbed or left intact. The actions of PTH on isolated aortic tissue and VSM cells from hypertensive and hypertensive/hyperparathyroid rats will also be examined. Serum calcium, magnesium and circulating immunoreactive PTH levels will be examined in these animals and correlated with age, blood pressure and vascular tissue responsiveness to PTH. These results will help to illucidate any possible physiological role of PTH in blood pressure regulation in the normotensive and hypertensive states.
