Sodium chloride as regulator of renal prostaglandin E2 production in patients with essential hypertension.

The effect of dietary sodium intake (5 days' low salt, 4 days' high salt) on 24-h urinary prostaglandin E2 (PGE2) and prostaglandin F2 alpha (PGF2 alpha) excretion, blood pressure (BP), and plasma renin activity (PRA) was evaluated in 16 patients with essential hypertension. Sodium restriction significantly increased urinary PGE2 excretion (p less than 0.05) from 151 +/- 76 to 328 +/- 94 ng/24 h, while high salt intake reduced renal PGE2 production to 114 +/- 41 ng/24 h (p less than 0.05). There was a moderate but not significant increase in urinary PGF2 alpha excretion on the low salt regimen, which was reversed under high salt diet. Systolic and diastolic blood pressure fell from 162 +/- 11 to 145 +/- 10 mm Hg, i.e., 102 +/- 6 to 90 +/- 9 mm Hg on low sodium intake (35 mEq/day) and returned to levels close to control after 4 days on a high salt diet (250 mEq/day). Under low salt conditions, PRA increased significantly (p less than 0.001) from 0.83 +/- 0.33 to 2.82 +/- 1.12 ng AI/ml/h and fell to 0.45 +/- 0.31 ng AI/ml/h on high salt regimen (p less than 0.001). The results demonstrate that dietary sodium chloride intake modulates renal PGE2 production in patients with essential hypertension. The depressed PGE2 production under high salt conditions may play a role in regulation of renal vascular resistance and influence sustainment of chronic hypertension disease.