Effect of calcium supplementation on the vascular sensitivity to angiotensin II in pregnant women

Abstract

Pregnant women destined to develop pregnancy-induced hypertension lose refractoriness to the pressor effects of infused angiotensin II. The effect of calcium supplementation on the vascular sensitivity to angiotensin II was investigated in pregnant women. We administered orally 600 mg of calcium L-aspartate daily to 22 pregnant women from 20 weeks of gestation to delivery. The values for the effective pressor dose of angiotensin II in the calcium-supplemented women were compared with those in 72 nonsupplemented pregnant women. The vascular sensitivity was significantly decreased after calcium supplementation. The values for the effective pressor dose of angiotensin II in the calcium-supplemented patients were 18.1 +/- 1.2 ng/kg/min at 20 weeks of gestation, 32.2 +/- 2.6 ng/kg/min at the twenty-sixth week, 41.1 +/- 3.4 ng/kg/min at the thirtieth week, and 25.9 +/- 2.9 ng/kg/min at the thirty-sixth week (mean +/- SEM), while those in the nonsupplemented patients were 17.3 +/- 1.2, 17.7 +/- 1.6, 17.6 +/- 1.2, and 15.0 +/- 1.6 ng/kg/min, respectively. Assessment of the changes in the effective pressor dose of angiotensin II in the individual patients indicated that the percentile changes from 20 weeks of gestation in the calcium-supplemented patients were also significantly greater than those in 22 nonsupplemented patients. These findings suggest that calcium supplementation tends to reduce the vascular sensitivity in pregnancy. The present dosage of calcium did not affect the blood chemical parameters and did not reduce the blood pressure. The incidence of pregnancy-induced hypertension in the calcium-supplemented patients was 4.5%, which was smaller than that (21.2%) in the nonsupplemented patients. Although there is no clear explanation of the mechanisms involved in such an effect of calcium, the present results do provide evidence to support the idea that oral calcium intake can prevent the onset of pregnancy-induced hypertension.