The effects of sodium and calcium in clinical hypertension: mediating role of vitamin D metabolism.

On the basis of this work, we believe it is reasonable to suggest that calcium regulating hormones in general, and 1,25 dihydroxyvitamin D in particular, contribute to the pathophysiology of human essential hypertension, especially salt sensitive forms. As such, levels of plasma renin activity, circulating ionized calcium, and serum 1,25 D levels both contribute to and serve as predictors of dietary salt-sensitivity and the potential benefit of increased oral calcium intake. Mechanistically, the different metabolic set points of these factors, determined on a genetic and/or environmental basis, serve to determine the heterogeneous blood pressure responses to similar dietary and mineral intakes. In this scheme, these monovalent and divalent ion regulating hormones transduce environmental mineral signals at the cellular level, thus determining their ultimate blood pressure effects. The cellular mechanism by which these altered metabolic hormonal set points serve to shift levels of intracellular cytosolic free calcium and other critical determinants of blood pressure, are the focus of current research.