Arachidonic Acid Metabolites, Other Inflammatory Mediators and Intestinal Ion Transport

Comment on paper by Schleihauf et al.

W.K. MacNaughton

I was intrigued by your paper and particularly impressed by both the complexity of the CYP system and the relative paucity of data in the intestine.  I have a few questions.

First, since 11,12-EET can affect Ca sensitive Cl channels, is there evidence for an effect on intestinal epithelial chloride secretion, as there is for 5,6-EET?  If so, is it also dependent upon cyclooxygenase activity (ie. blocked by indomethacin)?  

In a related question, is the effect of indomethacin on 5,6-EET-induced secretion due to cyclooxygenase inhibition, or could it be due to indomethacin's effects on intracellular Ca?  What concentration of indo was used to blocked the effect of 5,6-EET?

If the effect of 5,6-EET is really due to another arachidonic acid metabolite, where do you speculate the site of action of 5,6-EET is?  My guess would be subepithelial myofibroblast, but this is based on current dogma, not on any evidence that I have seen.

Finally, does 5,6-EET act at a known receptor?  Do the EETs act at prostaglandin receptors?

I look forward to seeing your responses to any or all of these questions.  

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