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Relationship between the chemical structure of prostaglandins and their vasoactivities in dogs
Author(s) -
NAKANO J.
Publication year - 1972
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.1476-5381.1972.tb07238.x
Subject(s) - vasodilation , chemistry , prostaglandin , coronary vasodilator , prostaglandin e , prostaglandin e1 , pharmacology , medicine , endocrinology , stereochemistry , biochemistry
Summary1 The relationship between the chemical structure and the direct vasoactivity of different prostaglandins administered intra‐arterially was studied in the dog hindlimb preparation. 2 All of the prostaglandins studied, except PGF 1α and PGF 2α , caused a dose related decrease in the femoral arterial perfusion pressure in dogs in which the femoral arterial blood flow was kept constant, indicating the direct vasodilator action of these prostaglandins. 3 Among the prostaglandins studied, PGE 1 is the most potent vasodilator. Comparing the chemical structure and vasodilator action of PGE 1 with those of different prostaglandins, the following conclusions can be made: 4 The formation of the Δ 5 double bond in PGE 1 causes no change in its vasodilator activity, whereas the saturation of the Δ 13 double bond of PGE 1 slightly reduces its activity. 5 The alterations in the orientation and length of the carboxyl and alkyl side chains reduce markedly the vasodilator action of PGE‐ and PGA‐compounds. 6 The presence of a carbonyl group at C9 is the most important requirement for the potent vasodilator action of PGE 1 . On the other hand, the presence and S‐configuration of a hydroxyl group at C15 are essential for the intrinsic action at the receptor sites in the vascular smooth muscle, but may not be responsible for the vasodilator action. 7 The esterification of PGE 1 or PGE 2 and a triple bond formation and the replacement of C7 with oxygen in prostaglandin appear to reduce or abolish their vasodilator action.