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Under basal conditions prostaglandin (PG) E2-excretion was significantly lower in 35 patients with essential hypertension studied than in 22 age- and sex-matched controls (p less than 0.02). PGF 2 alpha--excretion was similar in both groups. Within the first 15 minutes after furosemide i.v., PGE2-excretion rose substantially less in the patients than in the controls (p less than 0.001), while the increase in PGF 2 alpha-excretion was not different for both groups. The coincident rise of plasma renin activity was significantly lower in the hypertensive (167% +/- 11, SEM) than in the normotensive (386% +/- 46) group (p less than 0.001). Our results support the assumption that a decrease in renal cortical (vascular?) synthesis of vasodilatating PG's may be the cause for both, the diminished secretion of renin and the increase of vascular resistance in the kidney, which are often associated in essential hypertension.
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