Prostaglandins

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The most diverse group of autocrine regulators are the prostaglandins. These twenty-carbon-long fatty acids contain a five-membered carbon ring. Prostaglandins are members of a family called the eicosanoids (from the Greek eicosa = twenty), which are molecules derived from the precursor arachidonic acid. Upon stimulation by hormones or other agents, arachi-donic acid is released from phospholipids in the plasma membrane and may then enter one of two possible metabolic pathways. In one case, the arachidonic acid is converted by the enzyme cyclooxygenase into a prostaglandin, which can then be changed by other enzymes into other prostaglandins. In the other case, arachidonic acid is converted by the enzyme lipoxy-genase into leukotrienes, which are eicosanoids that are closely related to the prostaglandins (fig. 11.34).

Prostaglandins are produced in almost every organ and have been implicated in a wide variety of regulatory functions. The study of prostaglandins can be confusing because of the diversity of their actions, and because different prostaglandins may exert antagonistic effects in some tissues. For example, the smooth muscle of blood vessels relaxes (producing vasodilation) in response to prostaglandin E2 (abbreviated PGE2) and PGF2a; these effects promote reddening and heat during an inflammation reaction. In the smooth muscles of the bronchioles (airways of the lungs), however, PGF2a stimulates contraction, contributing to the symptoms of asthma.

The antagonistic effects of prostaglandins on blood clotting make good physiological sense. Blood platelets, which are required for blood clotting, produce thromboxane A2. This prostaglandin promotes clotting by stimulating platelet aggregation and vasoconstriction. The endothelial cells of blood vessels, by contrast, produce a different prostaglandin, known as PGI2 or prostacyclin, whose effects are the opposite—it inhibits platelet aggregation and causes vasodilation. These antagonistic effects

> Phospholipids of j plasma membrane

Arachidonic acid

Lipoxygenase ^ a Cyclooxygenase

PGG2

Leukotrienes

Inflammation

Bronchoconstriction; vasoconstriction; capillary permeability

Antiplatelet aggregation

Vasodilation

PGH2

pgi2

pge2

PGF2a

txa2

Antiplatelet aggregation

Smooth muscle relaxation

Smooth muscle contraction

Smooth muscle relaxation

Vasodilation

Smooth muscle contraction

Vasoconstriction

Platelet aggregation

Vasoconstriction

Figure 11.34 The formation of leukotrienes and prostaglandins. The actions of these autocrine regulators (PG = prostaglandin; TX = thromboxane) are summarized.

318 Chapter Eleven ensure that, while clotting is promoted, the clots will not normally form on the walls of intact blood vessels.

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