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 (UCa) 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.
|Original language||English (US)|
|State||Published - Jan 1 1983|
- Calcium balance vasodilation
- Hypertensive rat
ASJC Scopus subject areas
- Internal Medicine