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Calcium metabolism and familial risk of hypertension
D E Grobbee1, I M van Hooft, A Hofman
1Department of Epidemiology and Biostatistics, Erasmus University Medical School, Rotterdam, The Netherlands.
Insights
Disturbances in calcium metabolism may precede high blood pressure, suggesting a genetic link in familial hypertension. These findings highlight calcium
Area of Science:
- Cardiovascular Research
- Endocrinology
- Nutritional Science
Background:
- Observational studies link low dietary calcium intake to increased risk of primary hypertension.
- Subgroups of hypertensive patients exhibit indicators of relative calcium deficiency, though these may be secondary to elevated blood pressure.
Purpose of the Study:
- To investigate calcium metabolism disturbances in the early, pre-hypertensive phase of primary hypertension.
- To explore potential genetic links between calcium metabolism and familial hypertension.
Main Methods:
- Utilized the Dutch Hypertension and Offspring Study, focusing on young normotensive subjects with and without a family history of hypertension.
- Assessed calcium metabolism indicators, including serum ionized calcium and parathyroid hormone (PTH) levels.
Main Results:
- Identified disturbances in calcium metabolism during the early phase of primary hypertension, potentially preceding blood pressure elevation.
- Observed reduced serum calcium and increased plasma parathyroid hormone (PTH) [1-84] in offspring of hypertensive parents, indicating altered calcium balance.
- Suggests calcium metabolism changes may characterize familial hypertension and indicate a genetic basis for calcium-sensitive hypertension.
Conclusions:
- Calcium metabolism disturbances appear to be present in the early stages of primary hypertension and may precede its development.
- Findings support the hypothesis that altered calcium metabolism is a characteristic of familial hypertension, potentially reflecting a genetic predisposition.
- Calcium balance in prehypertensive individuals may be maintained through elevated circulating PTH levels.
Abstract:
There is circumstantial evidence that disturbances of calcium metabolism are implicated in primary hypertension. From a large number of observational epidemiological studies, data have shown that a low dietary calcium intake increases the risk for high blood pressure. There is no general sensitivity for the effects of inadequate calcium intake, but subgroups of hypertensive patients have been described characterized by reduced serum ionized calcium levels, increased urinary excretion of calcium, raised intracellular calcium levels, reduced cellular membrane calcium binding, and other indicators of a relative calcium need. Some of these changes, however, may be secondary to blood pressure elevation. The family history approach enables to study the pathophysiology of early primary hypertension, at a stage at which blood pressure differences between future hypertensive subjects and normotensive subjects are still limited. In the Dutch Hypertension and Offspring Study, young normotensive subjects were studied selected on the basis of presence or absence of familial predisposition for hypertension. The findings show that disturbances in calcium metabolism are present in the early phase of primary hypertension and may precede the development of high blood pressure. Moreover, they suggest that changes in calcium metabolism may be a characteristic of familial hypertension and could reflect a genetic basis for calcium sensitive hypertension. The presence of a relatively reduced serum calcium and increased plasma PTH [1-84] level in the offspring of hypertensive parents indicates that calcium balance in prehypertensive subjects is maintained at a higher level of circulating PTH. The implications of these findings in relation to other available data are discussed.