Although supplemental calcium typically lowers blood pressure in subjects with salt-sensitive, low-renin hypertension - presumably by down-regulating increased production of parathyroid hormone (PTH) and/or parathyroid hypertensive factor (PHF) - its impact on the blood pressure of unselected hypertensive or normotensive subjects, as assessed by meta-analyses, appears to be trivial at best. This suggests that calcium may actually raise blood pressure a bit in some patients with high-renin hypertension, a prediction that is borne out in rodent models of this disorder. There is limited clinical evidence that long-term calcium supplementation tends to raise plasma renin activity; this finding, if valid, could evidently rationalize the equivocal clinical impact of calcium on blood pressure. Salt restriction likewise boosts renin production, and this effect tends to most notable in subjects whose blood pressure fails to decline during low-salt diets. Two clinical groups have demonstrated that salt restriction has a larger and more consistently beneficial impact on the blood pressure of hypertensives when they concurrently are treated with ACE inhibitors - evidently because the physiological impact of the associated rise in renin is blunted. Analogous logic suggests that calcium supplementation may be more beneficial for hypertensives in the context of ACE inhibition or blockade of angiotensin II receptors; this supposition that can readily be tested clinically. The imminent availability of safe nutraceutical ACE inhibitors may make it more feasible for the general public to benefit from these therapeutic/preventive possibilities.