Salt intake and blood pressure in humans.

Abundant evidence exists to link the dietary intake of sodium to the development of high blood pressure and the potential occurrence of cardiovascular consequences including stroke, congestive heart failure and other forms of cardiovascular disease as well as renal failure. Not all individuals are sensitive to the blood pressure-raising effects of sodium. Genetic or acquired factors may determine an individual's ability to handle the sodium load. In sodium-sensitive hypertensives, modest dietary sodium restriction is beneficial in both reducing blood pressure and in controlling the elevated pressure with medication. A role for potassium and/or calcium with respect to the effects of sodium is an intriguing area of current inquiry.

Hypokalemia, normal blood pressure, and hyperreninemia with hypoaldosteronism.

The etiology of persistent hypokalemia and renal potassium loss was investigated in three children. Each had normal blood pressure but low plasma aldosterone values in relation to elevated plasma renin activity. None had a history of licorice abuse, laxative or diuretic use, persistent vomiting or diarrhea, pyelonephritis, or diabetes insipidus. Additional studies in one patient showed low prostaglandin E excretion and a normal platelet aggregation response to epinephrine and ADP. Although certain aspects of this condition resemble Bartter syndrome, the low concentrations of aldosterone and the absence of evidence for mineralocorticoid excess suggest a previously undescribed syndrome.