Calcemic response to parathyroid hormone in spontaneously hypertensive rats: role of calcitriol.

Spontaneously hypertensive rats (SHR) display lower ionized calcium (Pca++) concentrations when compared with normotensive Wistar Kyoto rats (WKY). This could be attributable to renal wasting of calcium, decreased intestinal calcium absorption, or decreased bone resorption, processes that are integrated by the parathyroid hormone (PTH) and vitamin D systems. We have studied the calcemic response to PTH infusion (3 U/hr/100 gm) for 5 hours in 13-week-old SHR and WKY. Pre-PTH Pca++ concentration of nonfasted SHR (4.68 +/- 0.06 mg/dl, N = 8) was significantly lower than that of WKY (4.84 +/- 0.03, N = 8, P less than 0.05). Pca++ concentration rose in both nonfasted WKY and SHR at the end of PTH infusion, but the increment of Pca++ in SHR (0.29 +/- 0.05 mg/dl, N = 8) was lower than that in WKY (Pca++, 0.60 +/- 0.07 mg/dl, N = 8, P less than 0.01). Urinary calcium excretion (UcaV) and creatinine clearances (Ccr) before and after PTH infusion were not different between WKY and SHR. Despite an increased filtered load of calcium, UcaV was not greater in either WKY or SHR during the PTH infusion. Pretreatment of SHR with calcitriol 50 ng intravenous bolus injection, which had no effect on Pca++ concentration (0.02 +/- 0.03 mg/dl, N = 7), corrected the lower calcemic response to PTH in SHR, and the Pca++ increment was no longer different between WKY (0.57 +/- 0.07 mg/dl, N = 7) and SHR (0.62 +/- 0.09, N = 7).(ABSTRACT TRUNCATED AT 250 WORDS)