Article date: January 1998
By: R A Borman, R Jewell, K Hillier, in Volume 123, Issue 2, pages 231-236
We have investigated the effects of platelet‐activating factor (PAF), an endogenous mediator of inflammation, on ion transport and prostaglandin synthesis in the human isolated colon.
Application of PAF to the serosal surface of human colonic mucosa induced a marked, concentration‐dependent increase in ion transport. Mucosal application was without effect.
The secretory response to PAF was significantly inhibited by prior application of a specific PAF receptor antagonist WEB 2170, indicating that the response is dependent on PAF receptor activation.
The response to PAF was attenuated by prior application of indomethacin or piroxicam, implicating products of the cyclo‐oxygenase pathway in the response.
The response to PAF was attenuated by the loop diuretic bumetanide, indicating an involvement of chloride ion secretion in the response.
Addition of PAF to the serosal surface induced a significant increase in serosal prostaglandin E2 (PGE2), but not 6‐oxo‐PGF1α release. There was no effect on mucosal application of PAF.
In summary, we have shown that PAF is a potent secretagogue in isolated preparations of human colon and that the response is dependent on a specific PAF receptor, cyclo‐oxygenase products and bumetanide‐sensitive chloride ion transport.
We have investigated the effects of platelet‐activating factor (PAF), an endogenous mediator of inflammation, on ion transport and prostaglandin synthesis in the human isolated colon.
Application of PAF to the serosal surface of human colonic mucosa induced a marked, concentration‐dependent increase in ion transport. Mucosal application was without effect.
The secretory response to PAF was significantly inhibited by prior application of a specific PAF receptor antagonist WEB 2170, indicating that the response is dependent on PAF receptor activation.
The response to PAF was attenuated by prior application of indomethacin or piroxicam, implicating products of the cyclo‐oxygenase pathway in the response.
The response to PAF was attenuated by the loop diuretic bumetanide, indicating an involvement of chloride ion secretion in the response.
Addition of PAF to the serosal surface induced a significant increase in serosal prostaglandin E2 (PGE2), but not 6‐oxo‐PGF1α release. There was no effect on mucosal application of PAF.
In summary, we have shown that PAF is a potent secretagogue in isolated preparations of human colon and that the response is dependent on a specific PAF receptor, cyclo‐oxygenase products and bumetanide‐sensitive chloride ion transport.
British Journal of Pharmacology (1998) 123, 231–236; doi:10.1038/sj.bjp.0701602
DOI: 10.1038/sj.bjp.0701602
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