Nitric oxide: orchestrator of endothelium-dependent responses.
Assays in vitro and in vivo were performed on extract from roots and leaves from the Valeriana prionophylla Standl. (VPR and VPF, resp.). In phenylephrine (1 μ M) precontracted rings, VPR (0.01-300 μ g/mL) induced a concentration-dependent relaxation (maximum response (MR) = 75.4 ± 4.0%, EC50 = 5.97 (3.8-9.3) μ g/mL, n = 6]); this effect was significantly modified after removal of the endothelium (EC50 = 39.6 (27.2-57.6) μ g/mL, P < 0.05). However, VPF-induced vasorelaxation was less effective compared to VPR. When rings were preincubated with L-NAME (100 μ M) or indomethacin (10 μ M), the endothelium-dependent relaxation induced by VPR was significantly attenuated (MR = 20.9 ± 2.3%, 34.2 ± 2.9%, resp., P < 0.001). In rings denuded endothelium, precontracted with KCl (80 mM), or in preparations pretreated with KCl (20 mM) or tetraethylammonium (1 or 3 mM), the vasorelaxant activity of VPR was significantly attenuated (MR = 40.0 ± 8.2, n = 5; 50.5 ± 6.0%; 49.3 ± 6.4%; 46.8 ± 6.2%; resp., P < 0.01). In contrast, neither glibenclamide (10 μ M), barium chloride (30 μ M), nor 4-aminopyridine (1 mM) affected VPR-induced relaxation. Taken together, these results demonstrate that hypotension induced by VPR seems to involve, at least in part, a vascular component. Furthermore, endothelium-independent relaxation induced by VPR involves K(+) channels activation, most likely due to BKCa channels, in the rat superior mesenteric artery.