Calcium metabolism and familial risk of hypertension

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 st 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 bleed 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 sad 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.