Cardiovascular effects induced by Cymbopogon winterianus essential oil in rats: involvement of calcium channels and vagal pathway
Article first published online: 19 MAR 2010
© 2010 Royal Pharmaceutical Society of Great Britain
Journal of Pharmacy and Pharmacology
Volume 62, Issue 2, pages 215–221, February 2010
How to Cite
De Menezes, I. A. C., Moreira, Í. J. A., De Paula, J. W. A., Blank, A. F., Antoniolli, A. R., Quintans-Júnior, L. J. and Santos, M. R. V. (2010), Cardiovascular effects induced by Cymbopogon winterianus essential oil in rats: involvement of calcium channels and vagal pathway. Journal of Pharmacy and Pharmacology, 62: 215–221. doi: 10.1211/jpp.62.02.0009
- Issue published online: 19 MAR 2010
- Article first published online: 19 MAR 2010
- Received August 3, 2009 Accepted November 3, 2009
- calcium channel;
- cardiovascular effects;
- Cymbopogon winterianus;
- essential oil;
- vagal pathway
Objectives This study has investigated the cardiovascular effects of the Cymbopogon winterianus essential oil (EOCW) in rats. C. winterianus is a plant used in folk medicine for the treatment of hypertension.
Methods For the measurement of haemodynamic and ECG parameters, male Wistar rats under anaesthesia were cannulated in the abdominal aorta and lower vena cava and electrodes were subcutaneously implanted in their paws. For an in-vitro approach, the rats were killed and the superior mesenteric artery was removed and cut into rings (1–2 mm). These rings were then mounted in organ baths containing Tyrode's solution at 37 °C and gassed with carbogen.
Key findings In rats, EOCW (1–20 mg/kg, i.v.) induced dose-dependent hypotension and tachycardia. These effects were not affected by L-NAME or indometacin, but were partially reduced after atropine administration. EOCW (20 mg/kg only) also induced bradycardia-associated sinoatrial blockade, junctional rhythm, and first-degree atrioventricular block, which was abolished after atropine administration or vagotomy. In arterial rings, EOCW (0.1–3000 μg/ml) induced relaxation of phenylephrine tonus that was not affected by removal of the endothelium. These relaxations were similar to those observed in rings without endothelium precontracted with KCl 80 mm. EOCW was able to antagonize the CaCl2 (30–300 μm) induced contractions in depolarizing solution (KCl 60 mm).
Conclusions These results demonstrated that EOCW induced hypotension and vasorelaxation. These effects appeared to be mainly mediated by Ca+2-channel blocking. Furthermore, the higher dose of EOCW induced transient bradycardia and arrhythmias due to a cardiac muscarinic activation secondary to a vagal discharge.