STIMULATION OF RENIN RELEASE BY 6‐OXO‐PROSTAGLANDIN E1 AND PROSTACYCLIN

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Abstract
Renin release induced by 6‐oxo‐prostaglandin E1 (6‐oxo‐PGE1) was compared to release in response to prostacyclin (PGI2) and 6‐oxo‐PGF1α in slices of rabbit renal cortex. Krebs‐Ringer medium bathing slices of renal cortex was collected for renin assay after four successive 20 min intervals (periods I‐IV). Renin release did not increase during periods I to IV in untreated slices. Agonists were added, only once, at the beginning of period III. Between periods III and IV, the incubation solution was aspirated and replaced with fresh medium. PGI2 increased renin release during period III while 6‐oxo‐PGE1 stimulated release during periods III and IV. 6‐oxo‐PGE1 stimulated renin release (24%–74%) in concentrations ranging from 1–33 μm while PGI2 stimulated release at 10 μm (60%) but not at 5 μm. 6‐oxo‐PGF1α, 10 μm, did not release renin during period III (period III, 9%), but caused a small rise in period IV (29%). 6‐oxo‐PGE1, unlike PGI2, was stable under the incubation conditions (pH 7.4, 37°C) as indicated by recovery of undiminished platelet anti‐aggregatory material after 20 min. In the rabbit kidney, activity of 9‐hydroxyprostaglandin dehydrogenase was greatest in the cortex and negligible in the papilla, corresponding to the zonal distribution of renin. The prominent and sustained in vitro renin releasing effect of 6‐oxo‐PGE1, as well as the cortical localization of enzyme activity capable of generating this stable prostacyclin metabolite, suggest that formation of 6‐oxo‐PGE1 may contribute to PGI2‐induced renin release and may explain the delayed stimulation caused by 6‐oxo‐PGF1α.