Red marine alga Bryothamnion triquetrum lectin induces endothelium-dependent relaxation of the rat aorta via release of nitric oxide

Abstract

We have investigated the vascular relaxant effects of the lectin from a red marine alga Bryothamnion triquetrum (BTL), in particular, the endothelial-dependency and the participation of a specific glycoprotein-binding site. BTL (1–100 μg mL−1) was applied to rat isolated aortic rings, with or without endothelium, tonically precontracted with phenylephrine (0.1 μm). Endothelium-dependent relaxation was assessed in the presence of indometacin (10 μm), l-nitro arginine methyl ester (L-NAME, 100 μm) and tetraethylammonium (TEA, 500 μm). For the involvement of the glycoprotein-binding site, BTL was assayed in presence of mucin (300 μg mL−1) or N-acetyl d-glucosamine (GlcNAc; 300 μg mL−1), a specific and non-specific lectin-binding sugar, respectively. BTL fully and concentration dependently relaxed preparations that possessed an intact endothelium (IC50 (concn producing 50% contraction) = 12.1 ± 1.6 μg mL−1), whereas no significant relaxation was observed in endothelial-denuded tissue. L-NAME, but not indometacin or TEA, completely inhibited the lectin relaxation, suggesting the involvement of nitric oxide (NO). The lectin in association with mucin, but not with GlcNAc, inhibited BTL-induced relaxation, implicating the involvement of the lectin binding site. Our data suggest that the relaxant effect of the red marine alga Bryothamnion triquetrum lectin on isolated aorta occurs via interaction with a specific lectin-binding site on the endothelium, resulting in a release of NO.