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  • Title: Pharmacology and biochemistry of the leukotrienes.
    Author: Piper PJ.
    Journal: Eur J Respir Dis Suppl; 1982; 122():54-61. PubMed ID: 6958494.
    Abstract:
    Leukotrienes (LTs) are metabolites of arachidonic acid formed by a 5-lipoxygenase. They are generated during immunological challenge or by reactions which involve changes in calcium levels. Their release is blocked by inhibitors of phospholipase A2 or lipoxygenase. LTB4 is a potent mediator of chemotaxis and of exudation of plasma. The peptidolipid LTs, LTC4, LTD4 and LTE4 are very active on a variety of types of smooth muscle. LTs C4 D4 and E4 contract guinea pig ileum (GPI), LTD4 being the most potent. LTC4 is converted to LTD4 on GPI. LTC+ and LTD4 cause bronchoconstriction in guinea pig in vivo and contract human bronchus, guinea pig trachea and parenchymal strips from guinea pig, human, rabbit and rat lung in vitro. LTB4 also contracted guinea pig parenchyma: the contraction of this tissue to all LTs is mainly due to thromboxane A2 released by LTs and is blocked by inhibitors of thromboxane synthesis. LTC4 and D4 cause prolonged hypertension guinea pig in vivo. However, they are vasoconstrictor in guinea pig skin in vivo and in guinea pig hearts in vitro, LTC4 being the most active. LTD4 is more active than LTC4 in causing exudation of plasma in guinea pig skin. FPL 55712 does not antagonise LTB4 but antagonises actions of LTC4 and D4 on GPI, and guinea pig parenchyma. FPL 55712 does not completely antagonise LTD4 in guinea pig heart or parenchyma from human, rabbit or rat lung. The actions of leukotrienes suggest they may contribute to the signs and symptoms of respiratory diseases such as asthma.
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