Renal prostaglandins in relation to sodium regulation and hypertension.

Abstract

The renal inner medulla is very rich in prostaglandins as well as in the enzymes that biosynthesize prostaglandins. When given intravenously, prostaglandin E or A will cause a natriuresis. Using a quick-freeze method one can measure the in vivo concentration of prostaglandins in the kidney. After a high NaCl intake for 2 weeks, the prostaglandin E2 (PGE2) concentration in rat kidneys decreases 40% below control. After 2 weeks of a low NaCl diet, the intrarenal PGE2 concentration approximately doubles. Blockers of prostaglandin synthesis have recently been shown to cause a natriuresis. These observations are compatible with the possibility that intrarenal PGE2 acts locally as an antinatriuretic hormone. Intrarenal prostaglandins may also have a role in certain forms of hypertension. The interstitial cells of the renal papilla appear to be able to secret antihypertensive humoral substances and can also synthesize prostaglandins. They have diminished numbers of cytoplasmic lipid granules in several forms of experimental hypertension. Moreover, using the quick-freeze method, the kidneys of "post-salt" hypertensive rats have a 36% lower intrarenal PGE2 level than is present in "post-salt" normotensive controls. Moreover, the kidneys from Kyoto spontaneously hypertensive rats have almost a three times greater intrarenal PGF2alpha concentration from Kyoto normotensive controls. The abnormal prostaglandin concentrations in these two types of hypertension may constitute key integral features of the control mechanisms through which the kidney brings about high blood pressure.