Abstract
The addition of prostaglandin (PG) D2 contracted helical strips of dog cerebral, coronary, renal and femoral arteries; the contraction was greatest in cerebral arteries. The contractile response of cerebral arteries was potentiated by aspirin and attenuated by polyphloretin phosphate. In the arterial strips contracted with PGF2α, PGD2 elicited a concetration-related relaxation; the relaxation was greatest in mesenteric arteries. In mesenteric arterial strips contracted with norepinephrine, a lesser degree of relaxation was induced, and in the K+-contracted arteries, only a contraction was induced. Treatment with PGD2 attenuated the contractile responses of cerebral and mesentric arteries to PGF2α or PGE2; this inhibitory effect was approximately 10 times greater in mesenteric arteries. However, the response to serotonin (for cerebral arteries) or norepinephrine (for mesenteric) was unaffected. It may be concluded that the heterogeneity of response to PGD2 of a variety of dog arteries is due to different contributions of vasoconstrictor and vasodilator mechanisms. PGD2 appears top share the mechanism underlying arterial contraction with PGF2α and PGE2, and interferes with the effect of these PG's possibly on receptor sites.
Published Version
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