Experimental and clinical data suggest an association between chronic
hyperparathyroidism and
hypertension, but acute infusion of
parathyroid hormone causes vasodilation and
hypotension. These observations imply that chronic and acute parathyroid states affect blood pressure through different mechanism(s), either by modification of vascular receptors or by an ionophoretic effect of
parathyroid hormone. The effect of parathyroid status induced by
dietary calcium manipulations or by surgical ablation of the parathyroid gland on the hypotensive response of
parathyroid hormone infusion was studied in rats. At 4 weeks of age 24 male rats were divided into four equal groups. Three groups were
sham-operated, and one group was thyroparathyroidectomized. Only the thyroparathyroidectomized group was treated with
thyroxine, 10 micrograms/kg/day. The control and thyroparathyroidectomized groups were raised on a 1.4%
calcium diet; the other two groups were raised on 0.005% and 2.8%
calcium diets. After 8 weeks on the diets,
parathyroid hormone was infused through a venous
cannula at 5 and 10 micrograms/kg doses and blood pressure was measured through arterial cannulas. The results indicate that
hyperparathyroidism and
hypocalcemia induced by the low
calcium diet attenuated the hypotensive response to
parathyroid hormone compared with responses in rats raised on a 1.4%
calcium diet. In hypoparathyroid rats (2.8% Ca diet) with
hypercalcemia, the hypotensive response was also reduced. However, in hypoparathyroid (thyroparathyroidectomized) rats with
hypocalcemia, the hypotensive response was enhanced. The data suggest that chronic parathyroid status, as well as
hypercalcemia, alters the hypotensive response to
parathyroid hormone infusion, presumably by altering the vascular
parathyroid hormone receptors or by some other mechanism.