A prostaglandin, not NO, mediates endothelium-dependent dilation in ventral aorta of shark (Squalus acanthias).

In mammals, the vascular endothelium releases a variety of paracrine factors, including the vasodilatory prostaglandin (PG)I2 and nitric oxide (NO), which is generally accepted as the major endothelium-derived relaxing factor (EDRF) in mammals. Current evidence for the vascular NO-EDRF system in fishes is contradictory. In addition, the role of PGs in the control of fish vascular tension is also unclear. We have utilized isolated rings of the ventral aorta of the spiny dogfish shark to examine the ability of various components of the NO system to dilate this vessel. Neither the NO precursor L-arginine, the NO donor sodium nitroprusside, nor NO itself dilated the rings. The Ca2+ ionophore A-23187 did produce an endothelium-dependent dilation that was not inhibited by the NO synthase inhibitor NG-nitro-L-arginine methyl ester but was inhibited by the cyclooxygenase inhibitor indomethacin, suggesting that PGs are involved. PGE1 and carbaprostacyclin, but not PGI2, produced concentration-dependent dilation, and intact aortic rings secreted five times as much PGI2 as PGE in both the unstimulated state and after stimulation with A-23187. Our data suggest strongly that a PG, most probably PGI2, is the EDRF in the ventral aorta of this shark species.