Nitric oxide-dependent vasodilatation by ethanolic extract of Hancornia speciosa via phosphatidyl-inositol 3-kinase

The vasodilator effect of the ethanolic extract of leaves from Hancornia speciosa Gomes (HSE) was studied in rat aortic rings. HSE produced a concentration-dependent vasodilatation (pIC50 = 5.6 ± 0.1), which was completely abolished in endothelium-denuded vessels. The endothelium-dependent vasodilatation induced by HSE was abolished by l-NAME (100 μM), a nitric oxide (NO) synthase inhibitor, but not atropine (1 μM; pIC50 = 5.6 ± 0.2), a muscarinic receptor antagonist, nor indomethacin (10 μM; pIC50 = 5.4 ± 0.2), a cyclooxygenase inhibitor. The concentration–response curve of HSE was significantly shifted to the left by superoxide dismutase (SOD; 300 U/mL). In addition, while SOD displaced the 3-morpholino-sidnonimine (SIN-1; P < 0.05) concentration–effect curve to the left, HSE (50 μg/mL) had no effect. Finally, wortmannin (0.3 μM), an inhibitor of phosphatidyl-inositol 3-kinase (PI3K), dramatically reduced the vasodilator effect of HSE. Together, these findings lead us to conclude that HSE induces a NO- and endothelium-dependent vasodilatation in rat aortic preparations, likely by a mechanism dependent on the activation of PI3K.