The levels of prostaglandins (PGS) E₂ and F₂α in different parts of the rabbit kidney were determined to observe the effect of sodium and indomethacin. After the pretreatment with injections of saline or with indomethacin, tissues from inner and outer medulla and cortex were separated, extracted, analyzed for PGE₂ and PGF₂α by radioimmunoassay. In the normal rabbit kidney, the greatest amount of PG was found in the inner medulla. Saline injections appeared to increase PGE₂ (but not PGF₂α), especially in the inner medulla. Repeated injections of saline, on the other hand, markedly reduced PGE₂ in the inner medulla but increased outer medullary PGE₂. Indomethacin reduced the production of PGS in all kidney segments. These results suggest the bidirectional effect of sodium on PG concentration in the rabbit kidney. Acute administration of sodium may directly stimulate the synthesis of PGE₂ in the inner medulla but chronic stimulation with sodium may alter the pattern of PGE₂ synthesis.

Prostaglandins (PGs) E₂ and F_2α in the rabbit kidney were determined by radioimmunoassay to study the effects of unilateral ureteral obstruction on intrarenal PGs. An increase of PGE₂ in the inner medulla was observed in the hydronephrotic kidney. When isotonic glucose solution was infused after the release of ureteral obstruction, an elevation of PGE₂ in the outer medulla occurred in the hydronephrotic kidney. Under water diuresis immediately following the release of obstruction, PGE₂ in the inner medulla showed significant correlations to urinary flow rate, urinary osmolar concentration and free water clearance. The present study indicates that PGE₂ in the inner medulla is enhanced by ureteral obstruction and may have a close relation to renal functional damage in mild hydronephrosis.

Prostaglandins (PGs) E₂ and F_2α in the rabbit kidney were determined in order to study the effects of unilateral ureteral occlusion for periods up to 6 weeks. A significant increase of PGE₂ concentration in the inner medulla of the obstructed kidney was always observed after ureteral occlusion of more than 24 h. In the contralateral kidney, PGE₂ in the inner medulla gradually decreased in proportion to the period of ureteral occlusion. The present results suggest that the enhanced PGE₂ may be a protective mechanism initiated to overcome the renal vasoconstriction after unilateral ureteral occlusion.

The unilateral renal artery in rabbits was constricted, and lipid droplet count in the medullary interstitial cells of the ‘opposite’ kidney was performed 1 week after surgery. Lipid droplet count in hypertensive rabbits was less than that in both nonhypertensive and normal rabbits and was inversely proportional to the mean blood pressure. Lipid droplet count was significantly correlated with the juxtaglomerular granulation index and the sodium content in the inner medulla. The present results suggest that, in the opposite kidney of rabbits hypertensive due to unilateral constriction of the renal artery, the enhanced release of prostaglandins and the washout of solute in the renal medulla may be induced as a response to increased perfusion pressure and elevated circulating angiotensin.

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