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Table 2 Differences between PGA and PGE
Effect
PGA
PGE
Indirect peripheral arteriolar dilation Minor degree
Direct peripheral arteriolar dilation
Major degree No effect
Marked decrease
Mechanism of hypotensive effect Metabolism by lung Renal oxidative metabolism and Na-K ATPase Effect on nonvascular smooth muscle
None
Contraction
BIOSYNTHESIS AND METABOLISM Prostaglandin Formation
The immediate precursors of prostaglandin synthesis are essential unsaturated fatty acids. It is now believed that they are needed in the diet because they play a pivotal role in being converted to prostaglandins (1,2). The precursor for PGE, and PGF, is 8, 11, 14-eicosatrienoic acid (dihomolinolenic acid), and that for PGE, and PGF, is 5, 8, 11, 14-eicosatetraenoic acid (arachidonic acid). It has also been shown that PGE and PGF, can be formed from 5, 8, 11, 14, 17-eicosapentaenoic acid. The transformation of unsaturated fatty acids to prostaglandins is catalyzed by PG synthetase, an enzyme specifically inhibited by essential fatty acid analogues and a number of anti-inflammatory agents, including indomethacin and aspirin. In the case of PGE, and PGF,, the mechanism of biosynthesis involves, (1) reduction of two of the double bonds in the fatty acid, (2) isomerization of the double bond with introduction of a molecular oxygen at C-9, 11, and 15 and (3) subsequent cyclization to the cyclic endoperoxide. The endoperoxide is then converted to either PGE,, or PGF,. The latter two compounds are not generally interconvertible, both being formed from the same endoperoxide precursor. A similar mechanism exists for the synthesis of PGE, from
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