Different responsiveness of a variety of isolated dog arteries to prostaglandin D3

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 PGF_2α, 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 PGF_2α 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 PGF_2α and PGE₂, and interferes with the effect of these PG's possibly on receptor sites.