Prostaglandin-9-ketoreductase activity in erythrocytes of normal and hypertensive subjects.
The PGE2/PGF2 alpha balance, controlled in part by prostaglandin-9-ketoreductase, seems to be involved in the regulation of sodium excretion by the kidney. A decreased PGE2/PGF2 alpha ratio has been observed in the urine of hypertensive subjects. This suggests that an alteration of prostaglandin metabolism might be involved in the pathogenesis of essential hypertension. In order to test this hypothesis, prostaglandin-9-ketoreductase (PG-9-KR) and prostaglandin-15-dehydrogenase (PG-15-DH) activities were measured in erythrocytes of normotensive controls and patients with essential hypertension. The two enzyme activities were highly correlated in the two groups, supporting the hypothesis that they are alternate expressions of a single enzyme. These two enzyme activities were not significantly different in hypertensive subjects as compared to controls. Human essential hypertension does not appear to be linked to a generalized defect of prostaglandin catabolic enzymes.
D000328:Adult; D000368:Aged; D004232:Diuretics / Q000627:therapeutic use; D004912:Erythrocytes / Q000187:drug effects / Q000201:enzymology*; D005260:Female; D006801:Humans; D006911:Hydroxyprostaglandin Dehydrogenases / Q000097:blood*; D006973:Hypertension / Q000097:blood / Q000188:drug therapy / Q000201:enzymology*; D007700:Kinetics; D008297:Male; D008875:Middle Aged; D012016:Reference Values
D004232:Diuretics; D006911:Hydroxyprostaglandin Dehydrogenases; C035858:prostaglandin-E2 9-reductase; C038661:15-hydroxyprostaglandin-D dehydrogenase (NADP+)