Milena Ramos Reis
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Abrahão Alves de Oliveira Filho
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Lilia Simone Urzedo Rodrigues
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Jaíse Paiva Araújo
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Priscilla Maria Pereira Maciel
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Assaysin vitroandin vivowere performed on extract from roots and leaves from theValeriana prionophyllaStandl. (VPR and VPF, resp.). In phenylephrine (1 μM) precontracted rings, VPR (0.01–300 μg/mL) induced a concentration-dependent relaxation (maximum response (MR) = 75.4 ± 4.0%, EC50= 5.97 (3.8–9.3)μg/mL,n=6]); this effect was significantly modified after removal of the endothelium (EC50= 39.6 (27.2–57.6)μg/mL,P<0.05). However, VPF-induced vasorelaxation was less effective compared to VPR. When rings were preincubated with L-NAME (100 μM) or indomethacin (10 μM), 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 μM), barium chloride (30 μM), 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 BKCachannels, in the rat superior mesenteric artery.