AJP - Renal Physiology, Vol 250, Issue 5 924-F929, Copyright © 1986 by American Physiological Society
Effects of hypercalcemia and parathyroid hormone on blood pressure in normal and renal-failure rats
K. Iseki, S. G. Massry and V. M. Campese
Hypertension is common in primary hyperparathyroidism, but the mechanisms
are not clear. Significant hypercalcemia induces elevation in blood
pressure (BP), whereas excessive parathyroid hormone (PTH) lowers BP.
However, in chronic renal failure (CRF) and secondary hyperparathyroidism,
the hypercalcemia-induced hypertension is more severe. We examined the
interaction between PTH and calcium on BP in normal rats and in those with
CRF. Calcium caused a dose-related rise in serum calcium and a rise in mean
arterial pressure (MAP). For a comparable rise in serum calcium, the
increment in MAP in parathyroidectomized (PTX) rats (7 +/- 3 mmHg) was
significantly lower (P less than 0.05) than in sham PTX rats (19 +/- 7.3
mmHg). In PTX rats receiving PTH, the MAP response to calcium infusion (17
+/- 2.4 mmHg) was similar to that in the sham PTX rats. The infusion of
similar amounts of calcium in CRF rats caused a greater rise in serum
calcium. In CRF-PTX rats, the changes in MAP during calcium infusion were
significantly lower (P less than 0.05) than in CRF-sham PTX animals,
despite similar rise in serum calcium. For a comparable rise in serum
calcium, the rise in MAP in CRF rats was greater than in normal rats. These
data suggest that the presence of PTH plays an important permissive role
for the hypertensive action of the hypercalcemia.
