Abstract
The actions of prostacyclin (PGI 2), prostaglandin E 2 (PGE 2), prostaglandin H 2 (PGH 2) and arachidonic acid have been examined on isolated coronary arteries from pigs. Arachidonate metabolites contracted this tissue, the order of potency being PGH 2 > PGE 2 > PGI 2 suggesting that the coronary vasoconstrictor effects of PGH 2 are limited by metabolism to PGI 2. Sodium arachidonate and linoleate weakly relaxed porcine coronary arteries, but the former induced a secondary prolonged contraction: only the contraction was abolished by indomethacin. Thus the relaxation induced by fatty acids does not depend on metabolism to prostaglandin-like substances.
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