The Calcium Deficiency Hypothesis of Hypertension: A Critique

Kaplan, Norman M.; Meese, Roderick B.

doi:10.7326/0003-4819-105-6-947

Cited by 51 publications

(11 citation statements)

References 63 publications

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“…21 In genetically hypertensive rats, calcium supplementation during the developmental phase of hypertension diminished the blood pressure increase. 22 In another study, however, genetically hypertensive rats fed a calcium-deficient diet did not show an increased blood pressure rise compared with rats fed a normal diet.…”

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confidence: 99%

Alterations in calcium metabolism in young people at risk for primary hypertension. The Dutch Hypertension and Offspring Study.

Hooft¹,

Grobbee²,

Frölich³

et al. 1993

Hypertension

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Several disturbances in calcium metabolism have been reported in primary hypertensive subjects. It is, however, not clear whether these alterations predate the development of hypertension or occur as a consequence of high blood pressure. We studied indexes of calcium metabolism in three groups of normotensive children with different familial predispositions for hypertension, based on parental blood pressure levels, with two, one, or no hypertensive parents. Plasma intact parathyroid hormone pressure regulation. In some hypertensive subjects, urinary excretion of magnesium may be decreased and show an inverse relation with blood pressure.16 Serum phosphate concentration is reported to be lower in hypertension and negatively related to blood pressure. 17Besides changes in serum and urinary electrolytes, raised circulating parathyroid hormone (PTH) levels have been demonstrated in hypertensive individuals. 1318 We reported previously that plasma intact PTH is raised in young hypertensive subjects compared with normotensive subjects of similar age, suggesting that alterations in calcium metabolism may be important in the early phase of primary hypertension. 1920Discussion remains as to whether changes in calcium metabolism are causally related to the development of high blood pressure. 21 In genetically hypertensive rats, calcium supplementation during the developmental phase of hypertension diminished the blood pressure increase. 22 In another study, however, genetically hypertensive rats fed a calcium-deficient diet did not show an increased blood pressure rise compared with rats fed a normal diet. 23 Parathyroidectomy in young genetically hypertensive rats, while keeping a normal serum calcium level, delayed the rise in systolic blood pressure for 42 weeks. 24 In humans, information on the part played by changes in calcium metabolism in the development of high blood pressure may be gained from comparison of

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confidence: 99%

Alterations in calcium metabolism in young people at risk for primary hypertension. The Dutch Hypertension and Offspring Study.

Hooft¹,

Grobbee²,

Frölich³

et al. 1993

Hypertension

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“…Even though total extracellular calcium levels, as measured in serum, tend to be higher in people with hypertension [7], it is unlikely that such slightly elevated levels could break through the normal protective mechanisms which maintain the usual 1,000-fold or greater differential between extracellular and intracellular calcium concentrations. Even though total extracellular calcium levels, as measured in serum, tend to be higher in people with hypertension [7], it is unlikely that such slightly elevated levels could break through the normal protective mechanisms which maintain the usual 1,000-fold or greater differential between extracellular and intracellular calcium concentrations.…”

Section: Possible Mechanismsmentioning

confidence: 98%

Calcium and blood pressure

Kaplan

1988

Cardiovasc Drug Ther

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A s the major intracellular signal for vascular contraction, calcium must be involved in the pathophysiology of hypertension. Until recently, however, it has been impossible to measure accurately the dynamic changes in the micromolar concentrations of intracellular calcium, in particular the less than 0.01% of the cell's calcium that is free and not bound. The availability of calcium-sensitive dyes such as quin 2 [1] and, even more recently, the use of fluorinated calcium chelators with nuclear magnetic resonance [2] has opened the way to accurate measurements of free cytosolic calcium during contraction of single cells.Therefore, the immediate future holds great promise for a major expansion of knowledge about the intimate relationships between calcium and blood pressure. What is now known is relatively crude and gross. Nonetheless, there is considerable evidence for disturbed handling of calcium by cells in hypertension.

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“…Kesteloot et al (1983) reported a negative and highly significant correlation between serum total calcium and 24-hr urinary sodium excretion in their epidemiological study. Moreover, Kaplan and Meese (1986) have suggested that the exaggerated natriuresis in hypertensives probably increases urinary calcium excretion and somewhat lowers the level of circulating calcium. Because it has been demonstrated (Richards et al 1985;Weidmann et al 1986) that urinary calcium output is increased by ANP infusion in normal volunteers, our finding of a significant inverse correlation between plasma ANP and serum calcium suggest that the increased ANP level in hypertensives may not only suppress PRA, but may also increase urinary calcium output and lower the serum level of calcium.…”

Section: Discussionmentioning

confidence: 99%