Dietary ca2+ prevents naci-induced exacerbation of hypertension and increases hypothalamic norepinephrine turnover in spontaneously hypertensive rats

Academic Article


  • Dietary calcium (Ca2+) supplementation lowers blood pressure in many forms of genetically mediated and experimentally induced hypertension. The present study tested the hypothesis that neuronal mechanisms underlie the blood pressure-lowering effect of dietary Ca2+ in NaCI-sensitive spontaneously hypertensive rats (SHR-S). SHR-S were fed one of the following diets: control (0.75% NaCI/0.68% Ca2+); high NaCI (8.00% NaCI/0.68% Ca2+); high Ca2+ (0.75% NaCI/2.00% Ca2+), and high NaCI/high Ca2+ (8.00% NaCI/2.00% Ca2+). SHR-S on the 8% NaCI diet for 2 weeks displayed significantly elevated blood pressure (161 ± 4 mmHg) compared with those on the control diet (139 ± 3 mmHg). Ca2+ supplementation prevented a rise in blood pressure in rats on the high-NaCI diet but did not alter blood pressure in rats consuming 0.75% NaCI. Plasma norepinephrine stores and turnover in the hypothalamus (anterior and posterior regions), brainstem (pons and medulla) and thoracic spinal cord were assessed using the dopamine-p-hydroxylase inhibitor 1-cyclohexyl-2-mercapto-imidazole. The 8% NaCI diets reduced anterior hypothalamic region norepinephrine stores and turnover. Concomitant Ca2+ supplementation restored norepinephrine turnover to normal, but did not alter norepinephrine stores in the anterior hypothalamic region. In other regions, no significant differences in norepinephrine content or turnover were observed among groups. In SHR that are resistant to high-NaCI diets (SHR-R), the diets did not alter blood pressure, and neither dietary NaCI nor Ca2+ supplementation affected norepinephrine turnover in any brain region studied. These data indicate that in SHR-S on a diet high in NaCI, Ca2+ supplementation may prevent the NaCI-induced exacerbation of hypertension by increasing norepinephrine turnover in the hypothalamus. © Current Science Ltd.
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    Author List

  • Wyss JM; Chen YF; Meng Q; Jin H; Jirikulsomchok S; Oparil S
  • Start Page

  • 711
  • End Page

  • 719
  • Volume

  • 7
  • Issue

  • 9