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Related Experiment Videos

Kinin effects on chloride secretion do not require eicosanoid synthesis.

A W Cuthbert, P V Halushka, D Kessel

    British Journal of Pharmacology
    |October 1, 1984
    PubMed
    Summary

    Essential fatty acid deficiency (EFAD) in rats impairs bradykinin-induced prostaglandin release in the colon. However, bradykinin still stimulates chloride secretion, indicating this process doesn't strictly require arachidonic acid metabolites.

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    Area of Science:

    • Gastroenterology
    • Physiology
    • Biochemistry

    Background:

    • Essential fatty acids are crucial for prostaglandin synthesis.
    • Bradykinin is a peptide that can stimulate colonic epithelial responses.
    • The role of prostaglandins in bradykinin-induced colonic secretion is not fully understood.

    Purpose of the Study:

    • To investigate the effects of essential fatty acid deficiency (EFAD) on bradykinin-induced responses in rat colonic epithelia.
    • To determine the contribution of prostaglandin production to bradykinin-mediated chloride secretion.

    Main Methods:

    • Measurement of short-circuit current (SCC) to assess electrogenic chloride secretion.
    • Quantification of immunoreactive prostaglandin E2 (iPGE2) and 6-keto PGF1 alpha release.

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  • Use of the cyclooxygenase inhibitor piroxicam to block prostaglandin synthesis.

    • Main Results:

    • Resting prostanoid release was significantly lower in EFAD rat colonic tissues compared to controls.
    • Bradykinin failed to increase prostanoid release in EFAD tissues but still induced 55% of the SCC response seen in controls.
    • The SCC response to bradykinin in EFAD tissues was unaffected by piroxicam.

    Conclusions:

    • Prostaglandin release contributes to, but is not essential for, bradykinin-induced electrogenic chloride secretion in rat colonic epithelia.
    • Bradykinin's effect on colonic secretion can occur independently of obligatory arachidonic acid metabolite production.