Abstract
Adaptive changes in the apparent amount of enzymes which synthesize and inactivate prostaglandins (PG) occur in a reciprocal manner. PG synthetase activity in several rat organs is reduced, but that of PG-metabolizing enzymes (prostaglandinases) is increased after treatment with anti-inflammatory steroids. In view of recent reports that the synthesis of PG-like substances may be influenced by plasma factors, the findings may be explained in whole or in part by the presence in varying amounts of substances which affect PG synthesis and inactivation in opposite directions. Rat plasma contains a protein factor(s) which inhibits the synthesis of PG and enhances their enzymatic breakdown in vitro and which is provisionally called prostaglandin reciprocal coupling factor (RCF). RCF is rapidly released in response to anti-inflammatory steroids, and its levels are altered in the 2 model pathophysiological states so far investigated.