FIGURE 16-17 Highly speculative model on the actions of PGEs versus enkephalin and glucocorticoids on pain production.

phospholipids. When an allergen interacts with IgE in the cell membrane (Figure 16-23), cell membrane methyltransferases are activated and catalyze the conversion of phosphatidylethanolamine to phosphatidylcholine. This produces changes in the membrane and in the orientation of phospholipids and results in opening of the calcium ion gate, or constitution of the gate as the case may be, so that calcium is taken up from the extracellular space. This series of events is similar to other receptor systems (see Chapter 1). The increased level of calcium-activated membrane phospholipase A2 results in the release of arachidonic acid from membrane phospholipid precursors. The cyclooxygenase-mediated metabolism of arachidonic acid would give rise to PGs, PGI2, or TX, whereas lipoxygenase-mediated events would form LT and monohydroxy fatty acids.

The LTs are of special interest because they possess the activities of the slow-reacting substance of anaphylaxis. The precursor to the LTs is hydroperoxyeicosate-traenoic acid (5-HPETE) (Figure 16-11). The LTs contain a 5-hydroxy group, three conjugated double bonds, and other polar substituents such as glutathione (GSH) (as in LTC4), as shown in Figure 16-11. The most potent LTs have one cis and two trans double bonds in the triene portion of the molecule (C-7). In most in vitro systems involving potency of smooth muscle contraction, the order of active substances is

16. Prostaglandins

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