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Alterations of dietary calcium intake as a therapeutic modality in essential hypertension
Insights
Calcium metabolism variations in hypertension are linked to blood pressure. Some patients have calcium deficiency, others excess, impacting salt sensitivity and oral calcium supplementation benefits.
Area of Science:
- Cardiovascular Medicine
- Endocrinology
- Nephrology
Background:
- Calcium metabolism alterations are observed in hypertensive disease, but their precise role in elevating blood pressure is not fully understood.
- Human hypertensive disease is heterogeneous, necessitating approaches that acknowledge this variability.
Purpose of the Study:
- To investigate calcium metabolism in essential hypertension using a renin system activity-based approach.
- To identify deviations in calcium metabolism that correlate with blood pressure regulation and salt sensitivity.
Main Methods:
- Analysis of plasma renin activity to categorize hypertensive patients.
- Measurement of circulating ionized calcium and calcium-regulating hormones.
- Assessment of blood pressure response to dietary salt and oral calcium supplementation.
Main Results:
- Identified parallel deviations in plasma renin activity, ionized calcium, and calcium-regulating hormones, indicating calcium deficiency or excess in different hypertensive groups.
- These deviations predict blood pressure sensitivity to dietary salt and identify candidates for calcium supplementation.
- Calcium demonstrated enhanced antihypertensive effects in low renin subjects with lower ionized calcium and higher 1,25-dihydroxyvitamin D, and in those with high salt intake.
Conclusions:
- Calcium metabolism and its hormonal regulation are implicated in the renin-angiotensin system and the pathophysiology of hypertension.
- Specific calcium metabolic profiles can predict response to dietary salt and calcium supplementation in hypertensive individuals.
- Further research into calcium-regulating hormones' role in hypertension is warranted.
Abstract:
Alterations of calcium metabolism in hypertensive disease have been increasingly observed, although the specific manner in which these alterations contribute to the increased blood pressure remains unclear. We have studied calcium metabolism in essential hypertension and have adopted an approach based on analysis of renin system activity, which emphasizes the heterogeneity of human hypertensive disease. With this approach we have defined parallel deviations of plasma renin activity, circulating ionized calcium, and calcium-regulating hormones, which suggest a calcium deficiency in some hypertensives and, an excess of calcium in others. These deviations can be used to predict and may mediate the blood pressure sensitivity of hypertensives to dietary salt, and may also target those individuals most likely to benefit from oral calcium supplementation. Calcium itself has enhanced antihypertensive effects in low renin subjects, having lower ionized calcium and higher endogenous 1,25-dihydroxyvitamin D values, and in subjects on higher dietary salt intakes. Calcium may alter pressure, at least in part, by suppressing endogenous vitamin D metabolites and by stimulating calcitonin secretion. We hypothesize that calcium-regulating hormones participate in the physiology of the renin-angiotensin system and in the pathophysiology of human hypertension.