Moderate cooling and responses to various alpha-adrenergic agonists in canine cutaneous veins

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Regulation of nitric oxide-like activity by prostanoids in smooth muscle of the canine saphenous vein.

1. Organ bath experiments and measurements of prostanoids were performed to investigate the presence of nitric oxide synthase in venous smooth muscle and its interaction with cyclo-oxygenase. 2. In rings of canine saphenous vein without endothelium, the inhibitor of cyclo-oxygenase, indomethacin (10 microM), induced contraction. NG-nitro-L-arginine (100 microM) (L-NOARG), an inhibitor of nitric oxide synthase did not affect the tone of rings of canine saphenous vein when administered alone. However, in the presence of indomethacin L-NOARG (100 microM) induced further contraction. 3. Similar results were obtained in response to NG-monomethyl-L-arginine (L-NMMA)(300 microM or NG-nitro-L-arginine methylester (L-NAME)(100 microM). 4. When rings of canine saphenous vein without endothelium were contracted with phenylephrine (1 microM) instead of indomethacin, neither L-NOARG or L-NMMA induced further contraction. 5. When rings of canine saphenous vein without endothelium were contracted with noradrenaline (0.3 microM) in the presence of indomethacin (10 microM) plus L-NOARG (100 microM), a relaxation to L-arginine was observed. Transient relaxations to superoxide dismutase (150 u ml-1) were observed in all rings. 6. When rings of saphenous vein without endothelium were incubated with lipopolysaccharide (LPS) (100 micrograms ml-1) or interleukin-1 beta (10 u ml-1) the concentration-contraction curve to noradrenaline was not affected. 7. Rings without endothelium released prostaglandin E2 and prostaglandin I2, as measured by radioimmunoassay. The basal production was abolished by indomethacin and not affected by L-NOARG. 8. These results suggest that when cyclo-oxygenase is inhibited, a nitric oxide synthase activity is revealed in rings of canine saphenous vein without endothelium

In SHR aorta, calcium ionophore A-23187 releases prostacyclin and thromboxane A2 as endothelium-derived contracting factors

In mature spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY), acetylcholine and the calcium ionophore A-23187 release endothelium-derived contracting factors (EDCFs), cyclooxygenase derivatives that activate thromboxane-endoperoxide (TP) receptors on vascular smooth muscle. The EDCFs released by acetylcholine are most likely prostacyclin and prostaglandin (PG)H2, whereas those released by A-23187 remain to be identified. Isometric tension and the release of PGs were measured in rings of isolated aortas of WKY and SHR. A-23187 evoked the endothelium-dependent release of prostacyclin, thromboxane A2, PGF2α, PGE 2, and possibly PGH2 (PGI2 ≫ thromboxane A2 = PGF2α = PGE2). In SHR aortas, the release of prostacyclin and thromboxane A2 was significantly larger in response to A-23187 than to acetylcholine. In response to the calcium ionophore, the release of thromboxane A2 was significantly larger in aortas of SHR than in those of WKY. In both strains of rat, the inhibition of cyclooxygenase-1 prevented the release of PGs and the occurrence of endothelium-dependent contractions. Dazoxiben, the thromboxane synthase inhibitor, abolished the A-23187-dependent production of thromboxane A 2 and inhibited by approximately one-half the endothelium-dependent contractions. U-51605, an inhibitor of PGI synthase, reduced the release of prostacyclin elicited by A-23187 but induced a parallel increase in the production of PGE2 and PGF2α, suggestive of a PGH2 spillover, which was associated with the enhancement of the endothelium-dependent contractions. These results indicate that in the aorta of SHR and WKY, the endothelium-dependent contractions elicited by A-23187 involve the release of thromboxane A2 and prostacyclin with a most likely concomitant contribution of PGH2. Copyright © 2006 the American Physiological Society.link_to_subscribed_fulltex