Renal PGs in essential hypertension; the role of water-electrolyte shifts in their metabolism.
Reduced PG formation in the renal vascular bed and urinary tract with increased PGF2 alpha/PGE2 ratio and altered PG response to acute and chronic salt loads were revealed in 100 patients with EH of different severity. The experiment on 70 rats has shown that the above changes in renal PG can be related to the increased Na concentration in the renal parenchyma resulting in decreased biosynthesis of both PGs in the kidneys and increased PGE2 transformation into PGF2 alpha. Renal PG changes are reversible after sodiumuresis and diuresis induced by various diuretics and other agents. The role of renal prostaglandins (PG) in the pathogenesis of essential hypertension (EH) and regulation of water-electrolyte metabolism has been studied for many years (B. Scherer et al., B. Lee et al., K. Abe et al., J.C. McGiff et al.). Reduced urinary PGE2 excretion was observed in patients with elevated blood pressure, while normotensive rats and healthy subjects on a low salt diet, treated by furosemide, showed PGE2 excretion increase. Salt loads, according to different authors, reduced, increased or caused no changes in urinary PGE2 excretion, with PGE2-9-ketoreductase activity increased. The aim of the present paper was the study of PGE2 and PGF2 alpha content in renal veins, their urinary excretion, biosynthesis and renal metabolism. The study was performed on patients with EH and on experimental rats at different salt loads.
D000328:Adult; D000818:Animals; D004032:Diet; D015237:Dinoprost; D015232:Dinoprostone; D006801:Humans; D006911:Hydroxyprostaglandin Dehydrogenases / Q000378:metabolism; D006973:Hypertension / Q000503:physiopathology*; D007610:Kallikreins / Q000652:urine; D007668:Kidney / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D008861:Microsomes / Q000378:metabolism; D008875:Middle Aged; D011453:Prostaglandins / Q000652:urine*; D011458:Prostaglandins E / Q000096:biosynthesis; D011460:Prostaglandins F / Q000096:biosynthesis; D051381:Rats; D012965:Sodium Chloride
D011453:Prostaglandins; D011458:Prostaglandins E; D011460:Prostaglandins F; D012965:Sodium Chloride; D015237:Dinoprost; D006911:Hydroxyprostaglandin Dehydrogenases; C035858:prostaglandin-E2 9-reductase; D007610:Kallikreins; D015232:Dinoprostone