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STIMULATION OF RENIN RELEASE BY 6‐OXO‐PROSTAGLANDIN E 1 AND PROSTACYCLIN
Author(s) -
MCGIFF JOHN C.,
SPOKAS ERIC G.,
WONG PATRICK YK
Publication year - 1982
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1982.tb08766.x
Subject(s) - prostacyclin , endocrinology , medicine , chemistry , stimulation , renin–angiotensin system , renal cortex , prostaglandin , plasma renin activity , metabolite , incubation , prostaglandin e1 , kidney , prostaglandin e2 , biology , biochemistry , blood pressure
1 Renin release induced by 6‐oxo‐prostaglandin E 1 (6‐oxo‐PGE 1 ) was compared to release in response to prostacyclin (PGI 2 ) and 6‐oxo‐PGF 1α in slices of rabbit renal cortex. 2 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. 3 PGI 2 increased renin release during period III while 6‐oxo‐PGE 1 stimulated release during periods III and IV. 6‐oxo‐PGE 1 stimulated renin release (24%–74%) in concentrations ranging from 1–33 μ m while PGI 2 stimulated release at 10 μ m (60%) but not at 5 μ m . 6‐oxo‐PGF 1α , 10 μ m , did not release renin during period III (period III, 9%), but caused a small rise in period IV (29%). 4 6‐oxo‐PGE 1 , unlike PGI 2 , was stable under the incubation conditions (pH 7.4, 37°C) as indicated by recovery of undiminished platelet anti‐aggregatory material after 20 min. 5 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. 6 The prominent and sustained in vitro renin releasing effect of 6‐oxo‐PGE 1 , as well as the cortical localization of enzyme activity capable of generating this stable prostacyclin metabolite, suggest that formation of 6‐oxo‐PGE 1 may contribute to PGI 2 ‐induced renin release and may explain the delayed stimulation caused by 6‐oxo‐PGF 1α .