The Role of Renal Prostaglandin E in the Mechanism of the Exaggerated Fractional Na Excretion in Hypertensive Patients with Advanced Renal Disease
Prostaglandin E (PGE) is a vasodilatory and natriuretic substance which is synthesized in the renomedullary interstitial cell and collecting tubule.1–3 Previous experimental and theoretical studies have shown a reduced clearance of sodium and water in renal hypertension.4 On the other hand, it is well known that sodium excretion per nephron varies inversely with the number of constituent nephrons, and that reduction of renal excretory function due to renal parenchymal disease is associated with exaggerated fractional sodium excretion.5 Since PGE can induce natriuresis, there is a possibility that renal PGE may contribute to the mechanism of exaggerated fractional sodium excretion in hypertensive patients with end-stage renal disease. The present study was performed to investigate this possibility.
KeywordsPlasma Renin Activity Sodium Excretion Plasma Aldosterone Concentration Renal Hypertension Sustained Hypertension
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