Vasorelaxant effect of the flavonoid galangin on isolated rat thoracic aorta

Abstract

Here we investigated the effect of the flavonoid galangin in isolated rat thoracic aortic rings. Galangin (0.1–100 μM) induced relaxation in rings pre-contracted with phenylephrine (PE 1 μM) or with KCl (100 mM) or pre-treated with the nitric oxide synthase inhibitor Nω-nitro-L-arginine methyl ester ( L-NAME, 100 μM), the cyclooxygenase inhibitor indomethacin (10 μM) and the adenylate cyclase inhibitor, SQ 22,536 (100 μM). In another set of experiments, rat aortic rings were incubated with galangin (1–100 μM) and the contractile responses to PE (0.001–3 μM) or to KCl (60 mM) were evaluated. We also evaluated the effect of galangin (100 μM) on PE (10 μM)-induced contraction in a Ca 2+-free medium. Galangin relaxed aortic rings with or without endothelium. Galangin effect was significantly inhibited by L-NAME. Galangin inhibited the contractile response to PE, either in presence or in absence of external calcium, and to KCl. In the end, we also found that galangin caused nitric oxide (NO) release from aortic rings and abolished the increase in [Ca 2+] i triggered by PE or KCl in aortic smooth muscle cells, either in presence and in absence of external Ca 2+. Our results suggest that galangin reduces the contractility of rat aortic rings through an endothelium-dependent mechanism, involving NO, and also through an endothelium-independent mechanism, inhibiting calcium movements through cell membranes.