Kinin effects on chloride secretion do not require eicosanoid synthesis.
The actions of bradykinin on colonic epithelia from essential fatty acid-deficient (EFAD) rats has been examined. Electrogenic chloride secretion as short circuit current (SCC) and release of immunoreactive prostaglandin E2 (iPGE2) and i 6-keto PGF1 alpha have been measured. Resting release of prostanoids was significantly less in EFAD than in control tissues. Bradykinin, in a maximally effective concentration, produced no increase in prostanoid release in EFAD tissues in contrast to controls, while the SCC response was 55% of that in controls. In EFAD tissues the SCC response to bradykinin was the same whether or not the cyclooxygenase inhibitor piroxicam was present. EFAD tissues were not more sensitive to prostaglandins than control tissues. We conclude that while prostaglandin release contributes to the totality of the response to bradykinin, the latter's effect on electrogenic chloride secretion does not require the obligatory production of arachidonic acid metabolites.
D015121:6-Ketoprostaglandin F1 alpha / Q000378:metabolism; D000818:Animals; D002712:Chlorides / Q000378:metabolism*; D003106:Colon / Q000378:metabolism; D015232:Dinoprostone; D004537:Eicosanoic Acids / Q000096:biosynthesis*; D004848:Epithelium / Q000378:metabolism; D005228:Fatty Acids, Essential / Q000172:deficiency; D005260:Female; D066298:In Vitro Techniques; D007705:Kinins / Q000494:pharmacology*; D011458:Prostaglandins E / Q000378:metabolism; D051381:Rats
D002712:Chlorides; D004537:Eicosanoic Acids; D005228:Fatty Acids, Essential; D007705:Kinins; D011458:Prostaglandins E; D015121:6-Ketoprostaglandin F1 alpha; D015232:Dinoprostone