Pathophysiological states modify levels in rat plasma of factors which inhibit synthesis and enhance breakdown of PG.
We have shown recently that adaptive changes in the apparent amount of enzymes which synthesize and inactivate prostaglandins (PGs) occur in a reciprocal manner (see accompanying paper and refs 2-4). For example, 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, we wondered whether our 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. We show here that rat plasma contains a protein factor(s) which inhibits the synthesis of PGs and enhances their enzymatic breakdown in vitro and which we provisionally call prostaglandin 'reciprocal coupling factor' (RCF). Furthermore, RCF is rapidly released in response to anti-inflammatory steroids and its levels are altered in the two model pathophysiological states so far investigated.
D000818:Animals; D002432:Cecum / Q000201:enzymology; D002474:Cell-Free System; D016861:Cyclooxygenase Inhibitors; D003921:Diabetes Mellitus, Experimental / Q000097:blood / Q000201:enzymology; D006801:Humans; D008297:Male; D011453:Prostaglandins / Q000378:metabolism*; D051381:Rats; D012669:Seminal Vesicles / Q000201:enzymology; D013974:Thyroxine / Q000494:pharmacology
D016861:Cyclooxygenase Inhibitors; D011453:Prostaglandins; D013974:Thyroxine