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Inhibitors of prostaglandin dehydrogenase (Ph CL 28A and Ph CK 61A) increase output of prostaglandins from rat isolated lung
Author(s) -
Bakhle Y.S.,
Pankhania J.J.
Publication year - 1987
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.1476-5381.1987.tb11311.x
Subject(s) - endogeny , prostaglandin e2 , arachidonic acid , prostaglandin , chemistry , pharmacology , efflux , medicine , endocrinology , enzyme , biochemistry , biology
1 Two potent inhibitors of prostaglandin dehydrogenase (PGDH), Ph CL 28A and Ph CK 61A, have been investigated for their effects on prostaglandin catabolism and synthesis in rat isolated lung. 2 Both CL 28A (0.3 μ m ) and CK 61A (0.5 and 5 μ m ) markedly increased the survival of prostaglandin E 2 (PGE 2 ) and PGF 2α on a single passage through the pulmonary circulation. 3 Both inhibitors delayed the efflux of 14 C following injection of [ 14 C]‐PGE 2 through the pulmonary circulation. 4 Output of PGE 2 and PGF 2α but not that of 6‐oxo‐PGF 1α from exogenous arachidonic acid (AA) was increased by CL 28A. 5 Output of all three prostaglandins from endogenous AA stimulated by calcium ionophore A23187 was increased by CL 28A. 6 With CK 61A, output of 6‐oxo‐PGF 1α from exogenous AA was not increased but that from endogenous AA was increased by either concentration of this inhibitor. 7 We conclude that it is possible to increase output of biologically active prostaglandins from lung by preventing their inactivation in situ.8 The apparent selectivity of PGI 2 synthesis from endogenous AA to potentiation by the inhibitors may have therapeutic possibilities.