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What are the mechanisms by which increased dietary calcium intake lowers blood pressure in spontaneously hypertensive rats and patients with arterial hypertension?
What are the mechanisms by which increased dietary calcium intake lowers blood pressure in spontaneously hypertensive rats and patients with arterial hypertension?
This review highlights that while dietary calcium can lower blood pressure in certain hypertensive populations, the exact physiological mechanisms mediating this effect remain unknown.
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Absence of unifying mechanism for calcium's BP effect; leaves open targeted trials while precluding practice changes.
An increase in dietary calcium intake lowers blood pressure in spontaneously hypertensive rats and in some patients with arterial hypertension. The mechanisms by which this decrease come about are not clear. A membrane-stabilizing effect wrought by an increase in extracellular calcium would appear unlikely, since the increases in extracellular calcium concentration with increased dietary intake are minimal. Calcium regulatory hormones may be the mediators, and a cybernetic framework has been suggested. Striking defects have been reported in the calcium handling and hormonal household of the spontaneously hypertensive rat. However, a clear cut relationship in terms of a hormonal "template" has not yet been identified in prospective experiments. Data have been presented to show that increased calcium intake has a direct effect on regulatory areas in the brain. However, the mechanisms by which such a response would be mediated are entirely unknown. Increased calcium intake may induce natriuresis. It has been suggested that increased calcium intake helps the "salt sensitive"; however, prospective studies to this effect have not been presented. Increased calcium intake may induce phosphaturia. However, the evidence that blood pressure lowering effects are mediated by phosphate depletion are unconvincing. Some evidence suggests that increased calcium intake may influence local regulatory processes which in turn influences cell integrity and growth. At this point, a unifying hypothesis is not available. However, the clues to various possibilities are intriguing.
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Friedrich C. Luft (1990) studied this question.
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