Enhancement of contraction of rat mesenteric artery by acteoside: Role of endothelial nitric oxide

The present study describes the role of endothelium in the vascular response to purified acteoside from Ligustrum purpurascens in rat mesenteric arteries. In endothelium-intact rings, acteoside (3−50 μmol/L) enhanced phenylephrine-induced contraction without affecting the maximum response. This enhancement was absent in endothelium-denuded rings. Pretreatment with nitric oxide synthase (NOS) inhibitors, NG-nitro-l-arginine (l-NNA, 100 μmol/L) and NG-nitro-l-arginine methyl ester (l-NAME, 100 μmol/L), or a selective guanylyl cyclase inhibitor, 1H-[1,2,4]oxadiazolo[4,2-α]quinoxalin-1-one (ODQ, 10 μmol/L), increased both the sensitivity of vasoconstriction to phenylephrine and the maximal response. The enhancing effect of acteoside (30 μmol/L) was abolished in the presence of l-NAME, l-NNA, or ODQ. Tetraethylammonium (TEA+, 3 mmol/L), a putative K+ channel blocker, also abolished the effect of acteoside. CaCl2 (0.01−10 mmol/L) induced contractions in 50 mmol/L K+-containing Krebs solution. Neither acteoside ...