| SHORT COMMUNICATION |
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| Year : 2011 | Volume
: 43
| Issue : 6 | Page : 694-698 |
Chemical composition and vasorelaxant effect induced by the essential oil of Lippia alba (Mill.) N.E. Brown. (Verbenaceae) in rat mesenteric artery
Luana G Maynard1, Kátia C Santos1, Patrícia S Cunha1, André S Barreto1, Magna G Peixoto2, Fátima Arrigoni-Blank2, Arie F Blank2, Péricles B Alves3, Leonardo R Bonjardin1, Márcio R.V Santos1
1 Departamento de Fisiologia, Universidade Federal de Sergipe, São Cristóvão - SE, Brazil
2 Departamento de Agronomia, Universidade Federal de Sergipe, São Cristóvão - SE, Brazil
3 Departamento de Química, Universidade Federal de Sergipe, São Cristóvão - SE, Brazil
Correspondence Address:
Márcio R.V Santos
Departamento de Fisiologia, Universidade Federal de Sergipe, São Cristóvão - SE
Brazil
 Source of Support: FAPITEC-SE and CNPq, Brazil, Conflict of Interest: None  | Check |
DOI: 10.4103/0253-7613.89828
Objectives : To investigate the chemical composition and vasorelaxant effect of the essential oil of Lippia alba (EOLA) in rat mesenteric artery.
Material and Methods : Chemical composition of EOLA was investigated by gas chromatography-mass spectrometry (GC/MS). Vasorelaxant effect was evaluated in vitro in rat superior mesenteric artery rings.
Results : GC/MS analysis revealed the presence of 19 compounds, with geranial (48.58%) and neral (35.42%) being the major constituents. In intact rings precontracted with phenylephrine (Phe: 1 μM), EOLA (100-1000 μg/mL) induced relaxation, where the maximal effect (Emax) was 110.8 ± 10.8%. This effect was not modified after endothelium removal (Emax = 134.8 ± 16.5%), after tetraethylammonium (TEA) (Emax = 117.2 ± 4.96%), or in rings precontracted with KCl (80 mM) (Emax = 112.6 ± 6.70%). In addition, EOLA was able to inhibit the contraction caused by CaCl 2 and produced a small but significant (P<0.05) additional effect (from 70.5 ± 3.4 to 105.3 ± 13.5%, n = 5) on the maximal relaxation of nifedipine (NIF: 10 μM).
Conclusions : The results demonstrated that EOLA induces endothelium-independent vasorelaxation, which appears to be caused, at least in part, by blocking Ca 2+ influx through voltage-operated Ca 2+ channels.
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