Endothelium-dependent vasodilation induced by Hancornia speciosa in rat superior mesenteric artery

• Published in: Phytomedicine (Stuttgart) Vol. 14; no. 7; pp. 473 - 478
• Main Authors: Ferreira, H.C., Serra, C.P., Endringer, D.C., Lemos, V.S., Braga, F.C., Cortes, S.F.
• Format: Journal Article
• Language: English
• Published: Germany Elsevier GmbH 01-08-2007; Urban & Fischer Verlag
• Subjects: Angiotensin; Animal experimentation; Animals; Apocynaceae - chemistry; Cardiovascular agents; Dose-Response Relationship, Drug; EDHF; Endothelium; Endothelium - drug effects; Endothelium-derived relaxing factors; Glycosides; Hancornia speciosa; Hypertension; Indomethacin; Instrument industry; Male; Mesenteric Arteries - drug effects; Nitric oxide; Physiological aspects; Plant Extracts - chemistry; Plant Extracts - pharmacology; Plant Leaves - chemistry; Rats; Rats, Wistar; Resistance artery; Vasodilation; Vasodilation - drug effects; Brazil; United States; Hancornia speciosa; EDHF; Nitric oxide; Vasodilation; Resistance artery; Endothelium
• ISSN: 0944-7113; 1618-095X
• DOI: 10.1016/j.phymed.2006.11.008

The vasodilator effect of the ethanolic extract of leaves from
Hancornia speciosa Gomes (HSE) was evaluated in superior mesenteric artery rings. HSE produced a concentration-dependent vasodilation (IC
50=10.8±4.0
μg/mL) in arterial rings pre-contracted with phenylephrine, which was completely abolished in endothelium-denuded vessels. Endothelium-dependent vasodilation induced by HSE was strongly reduced by
l-NAME (100
μM), a nitric oxide (NO) synthase inhibitor, but neither by atropine, a muscarinic receptor antagonist (1
μM), nor by indomethacin (10
μM), a cyclooxygenase inhibitor. In rings pre-contracted with 80
mM KCl, the vasodilator effect of HSE was shifted to the right and was completely abolished in the presence of
l-NAME (100
μM). Similar effects were obtained in mesenteric rings pre-contracted with phenylephrine in the presence of KCl 25
mM alone or in addition to 100
μM
l-NAME. In addition, BaCl
2 (1
mM) dramatically reduced the vasodilation induced by HSE. Together, these findings led us to conclude that HSE induces an endothelium-dependent vasodilation in rat mesenteric artery, by a mechanism dependent on NO, on the activation of potassium channels and endothelium-derived hyperpolarizing factor release. Rutin, identified as a major peak in the HPLC fingerprint obtained for HSE, might contribute for the observed vasodilator effect, since it was able to induce an endothelium-dependent vasodilation in rat superior mesenteric arteries.