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 (pIC(50)=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 microM), a nitric oxide (NO) synthase inhibitor, but not atropine (1 microM; pIC(50)=5.6+/-0.2), a muscarinic receptor antagonist, nor indomethacin (10 microM; pIC(50)=5.4+/-0.2), a cyclooxygenase inhibitor. The concentration-response curve of HSE was significantly shifted to the left by superoxide dismutase (SOD; 300U/mL). In addition, while SOD displaced the 3-morpholino-sidnonimine (SIN-1; P<0.05) concentration-effect curve to the left, HSE (50 microg/mL) had no effect. Finally, wortmannin (0.3 microM), 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.