The effects of indomethacin and prostaglandins E2 and F2α on canine tracheal mucus generation

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Abstract
The effects of prostaglandins on respiratory smooth muscle are well known; however, their role in mucus generation has received little attention. This investigation was undertaken to study the actions of prostaglandin E2 (PGE2) and prostaglandin F2α (PGF2α) on secretion and synthesis of respiratory mucus glycoproteins. The method employed canine tracheal explants; radiochemical precursors were used in the culture media for labelling and quantitation of the secreted glycoproteins. Glycoprotein secretion was not significantly influenced by PGE2 (1×10−10 to 1×10−3 M) or PGF2α (1×10−8 to 1×10−4 M). However, PGF2α (1×10−3 M and 1×10−2 M), significantly stimulated glycoprotein secretion. The mechanism may have involved a contractile effect on myoepithelial cells of the submucosal glands. Synthesis of glycoproteins was significantly inhibited by PGF2α (1×10−5 M), indomethacin (1×10−6 M), and the combination PGF2α (1×10−5 M)/indomethacin (1×10−6 M). PGE2 (1×10−5 M) and arachidonic acid (1×10−5 M) were without effect. These data suggested that indomethacin inhibited glycoprotein synthesis by a mechanism other than an action on prostaglandin synthetase. In addition, because these agents inhibited synthesis of glycoproteins which were labeled with3H-glucosamine,35S-sulfate, and14C-serine, it appears that their action was primarily upon synthesis of the protein core.