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8 Cards in this Set

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Eicosanoid Agonists
Most eicosanoid effects appear to be brought about by activation of cell surface receptors (Table 18–1) that are coupled by the Gs protein to adenylyl cyclase (producing cyclic adenosine monophosphate [cAMP]) or by the Gq protein to the phosphatidylinositol cascade (producing inositol 1,4,5-trisphosphate [IP 3] and diacylglycerol [DAG] second messengers).
Eicosanoid Antagonists
As indicated in Figure 18–1, corticosteroids inhibit the production of arachidonic acid by phospholipases in the membrane. This effect is mediated by intracellular steroid receptors that, when activated by an appropriate steroid, increase expression of specific proteins capable of inhibiting phospholipase. Steroids also inhibit the synthesis of COX-2.
Corticosteroids
As indicated in Figure 18–1, corticosteroids inhibit the production of arachidonic acid by phospholipases in the membrane. This effect is mediated by intracellular steroid receptors that, when activated by an appropriate steroid, increase expression of specific proteins capable of inhibiting phospholipase. Steroids also inhibit the synthesis of COX-2
NSAIDs
Aspirin and other nonsteroidal (ie, noncorticosteroid) anti-inflammatory drugs inhibit cyclooxygenase and the production of the thromboxane, prostaglandin, and prostacyclin branches of the synthetic path
Celecoxib is the most selective COX-2 inhibitor available in the United States; meloxicam is also slightly COX-2-selective.
Inhibition of cyclooxygenase by aspirin, unlike that by other NSAIDs, is irreversible
Leukotriene Antagonists
Zileuton is a selective inhibitor of lipoxygenase and some cyclooxygenase inhibitors exert a mild inhibitory effect on leukotriene synthesis.
Zafirlukast and montelukast, inhibitors at the LTD4 receptor, are currently available for the treatment of asthma (Chapter 20).
Endogenous NO
Endogenous NO is synthesized by a family of enzymes collectively called nitric oxide synthase (NOS), Figure 19–1. These intracellular enzymes are activated by calcium influx or by cytokines. Arginine, the primary substrate, is converted by NOS to citrulline and NO
Drugs that cause endogenous NO release do so by stimulating its synthesis by NOS. Such drugs include muscarinic agonists, histamine, and certain other vasodilators (bradykinin, hydralazine).
Exogenous NO Donors
NO is released from several important drugs, including nitroprusside , nitrates, and nitrites. Release from nitroprusside occurs spontaneously in the blood in the presence of oxygen, whereas release from nitrates and nitrites is enzymatic and intracellular and requires the presence of thiol compounds such as cysteine. Tolerance may develop to nitrates and nitrites if endogenous thiol compounds are depleted.
NO Inhibitors
Although inhibitors of NO synthesis are of great research interest, none are currently in clinical use. NO can be inactivated by heme and hemoglobin, but application of this approach is in preclinical research.