Sodium is more important than calcium in essential hypertension.
There is much circumstantial and some direct evidence in humans to suggest that a high consumption of salt predisposes communities and individuals to the development of essential hypertension. Recent work has suggested possible mechanisms whereby a high salt intake could cause a rise in blood pressure in genetically susceptible persons. Restriction of salt intake in the diet lowers blood pressure in many subjects with high blood pressure and this fall in blood pressure is mediated in part by a diminished renin response to sodium restriction as hypertension develops. The effect of sodium restriction, like diuretics, is additive to most blood pressure lowering drugs, particularly those that inhibit the renin system such as beta-blockers and angiotensin converting enzyme inhibitors. Claims that a slight reduction in calcium intake may be important in the development of high blood pressure are disputed. Furthermore, no satisfactory hypothesis has been put forward to explain how a small reduction in dietary calcium intake could cause high blood pressure. Large increases in calcium intake have been reported to lower blood pressure in both normotensive and hypertensive humans. The three published studies, however, are not in agreement.
D000818:Animals; D001794:Blood Pressure; D002118:Calcium / Q000378:metabolism* / Q000502:physiology; D002136:Calcium, Dietary / Q000008:administration & dosage; D004039:Diet, Sodium-Restricted; D005110:Extracellular Space / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000209:etiology* / Q000503:physiopathology; D009318:Natriuresis; D051381:Rats; D012964:Sodium / Q000378:metabolism*; D012965:Sodium Chloride / Q000008:administration & dosage
D002136:Calcium, Dietary; D012965:Sodium Chloride; D012964:Sodium; D002118:Calcium