Role of endothelium in the response to prostaglandin H2 in isolated dog arteries.
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Prostaglandin (PG) H<SUB>2</SUB> produced a transient contraction followed by a relaxation in helical strips of dog coronary, mesenteric and renal arteries contracted with PGF<SUB>2α</SUB>. The contraction was in the order of mesenteric>renal>coronary artery. Removal of endothelium abolished the contraction in these arteries and significantly potentiated the relaxation only in mesenteric arteries. The relaxation was greater in mesenteric arteries than in renal and coronary arteries, denuded of endothelium. PGI<SUB>2</SUB>-induced relaxations were not influenced by endothelium denudation. In the arteries contracted with K<SUP>+</SUP>, PGH<SUB>2</SUB>-induced relaxations were attenuated, compared to those contracted with PGF<SUB>2α</SUB>. Treatment with ON03708, an antagonist of vasoconstrictor PGs, abolished the PGH<SUB>2</SUB>-induced contraction and potentiated the relaxation in the K<SUP>+</SUP>-contracted arteries. The relaxant response was suppressed by diphloretin phosphate, a PG receptor antagonist, as was the response to PGI<SUB>2</SUB>. PGH<SUB>2</SUB>-induced contractions in dog coronary, mesenteric and renal arteries would be due to vasoconstrictor PGs produced preferentially in the endothelium. However, production of PGI<SUB>2</SUB> from PGH<SUB>2</SUB> in endothelial and subendothelial tissues do not appear to differ.
- 公益社団法人 日本薬理学会の論文
公益社団法人 日本薬理学会 | 論文
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