Calcium Balance and Parathyroid Hormone Mediated Vasodilation in the Spontaneously Hypertensive Rat

The spontaneously hypertensive rat (SHR) exhibits multiple abnormalities of calcium metabolism. Parathyroid hormone (PTH) has been shown to be a potent vasodilator in the SHR as well as other animal species. The current study assessed the influence of short-term manipulation of Ca2 + balance on PTH-induced vasodilation in the SHR. At 16 weeks of age, seven male SHRs were placed on a 0.02% Ca²⁺(deficient) diet, and eight SHRs were fed a 4% Ca²⁺(supplemented) diet. Before and 2 weeks after the diet switch, blood and urine samples were obtained. Immediately thereafter, the SHRs received graded, bolus intravenous infusions of human (h)PTH 1-34 (0.1 to 100 μg/kg), and arterial pressure was monitored. The 4% SHR's serum total Ca²⁺rose (p < 0.001) but its serum ionized Ca²⁺was unchanged. Urinary Ca (U_Ca) increased (p < 0.005), and urinary cAMP declined (p < 0.05) in the 4% SHR. The 0.02% SHR's serum total and ionized Ca2 + were unchanged while their UClV actually increased (p < 0.05) and their urinary cAMP increased (p < 0.01). Both the 4% and 0.02% SHRs exhibited log-dose dependent (p < 0.001) depressor responses to hPTH 1-34. The 4% SHR, however, demonstrated greater (p < 0.01) sensitivity to and prolongation of (p < 0.01) this hypotensive action of PTH. We conclude that PTH is a potent depressor peptide in the SHR. Modification of Ca²⁺balance in the SHR will alter the dose response curve to PTH-induced vasodilation. Alterations in cellular Ca²⁺but not necessarily extracellular Ca²⁺appear to be functionally important in determining the vascular effects of hPTH 1-34.