Different responsiveness of a variety of isolated dog arteries to prostaglandin D2.

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 PGF2 alpha, PGD2 elicited a concentration-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 response of cerebral and mesenteric arteries to PGF2 alpha 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 responses to PGD2 of a variety of dog arteries is due to different contributions of vasoconstrictor and vasodilator mechanisms. PGD2 appears to share the mechanism underlying arterial contraction with PGF2 alpha and PGE2, and interferes with the effect of these PG's possibly on receptor sites.