Premium
INHIBITION OF THE PULMONARY INACTIVATION OF PROSTAGLANDINS in vivo BY DI‐4‐PHLORETIN PHOSPHATE
Author(s) -
CRUTCHLEY D.J.,
PIPER PRISCILLA J.
Publication year - 1975
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.1476-5381.1975.tb07569.x
Subject(s) - in vivo , prostaglandin , prostaglandin e2 , prostaglandin f2alpha , chemistry , pharmacology , endocrinology , medicine , antagonism , phloretin , prostaglandin antagonist , prostaglandins f , long term potentiation , biology , receptor , biochemistry , microbiology and biotechnology
1 Inactivation of prostaglandin E 2 in the pulmonary circulation of rabbits in vivo was measured by comparing the hypotensive effects of doses given intravenously and intra‐arterially. 2 Di‐4‐phloretin phosphate (DPP) 25–100 μg kg −1 min −1 inhibited the inactivation of prostaglandin E 2 in the pulmonary circulation. 3 These doses of DPP caused a marked shift to the left of the dose‐response curve to prostaglandin E 2 given intravenously but did not affect the dose‐response curve to prostaglandin E 2 given intra‐arterially. 4 Inhibition of pulmonary inactivation of prostaglandins E 2 and E 2α caused marked potentiation of their gastrointestinal effects. 5 At these doses antagonism of the hypotensive action of prostaglandin E 2 by DPP was seldom seen but the gastrointestinal effect of prostaglandin E 2α was sometimes antagonized. 6 After treatment with DPP 100 μg kg −1 min −1 , high doses of prostaglandin were sometimes lethal.