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Planta Med. 2001 Oct;67(7):638-43.

Cardiovascular effects of the essential oil of Mentha x villosa and its main constituent, piperitenone oxide, in normotensive anaesthetised rats: role of the autonomic nervous system.

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  • 1Departamento de Fisiologia e Farmacologia, Universidade Federal de Pernambuco, 50670-901, Recife, Pernambuco-PE, Brazil.


Cardiovascular effects of intravenous (i. v.) treatment with the essential oil of Mentha x villosa (EOMV) were investigated in pentobarbitone-anaesthetised rats. Additionally this study examines whether the major constituent of EOMV, piperitenone oxide (PO), is the active principle mediating EOMV-induced changes in mean aortic pressure (MAP) and heart rate (HR) and whether the autonomic nervous system is involved in the mediation of these cardiovascular effects. Two samples of EOMV have been tested: one contained 62.32% of PO (sample 1) and the other contained a higher percent (95.87%) of PO (sample 2). Intravenous injections of bolus doses (1 to 20 mg/kg) of both samples of EOMV elicited immediate and dose-dependent decreases in MAP and HR. These cardiovascular responses were also observed following i. v. injections of PO (1 to 20 mg/kg). However, maximal percent decreases in MAP and HR elicited by sample 2 of EOMV were significantly greater than those evoked by sample 1 of EOMV, while they were of the same order of magnitude as those elicited by PO. Pretreatment of rats with either bilateral vagotomy or i. v. methylatropine (1 mg/kg) did not modify significantly the hypotensive and bradycardic responses to EOMV. In contrast, pretreatment with i. v. hexamethonium (30 mg/kg) partially, but significantly, reduced the bradycardic effects of EOMV without affecting hypotension. The present study shows for the first time that i. v. treatment with EOMV in pentobarbitone-anaesthetised rats induces hypotensive and bradycardic effects, which appear mostly attributed to the actions of the major constituent of EOMV, PO. These cardiovascular effects appear to be independent since EOMV-induced bradycardia appears dependent upon the presence of an intact and functional sympathetic nerve drive to the heart, while EOMV-induced hypotension appears independent of the presence of an operational sympathetic nervous system. This suggests that hypotensive activity of EOMV may result from its vasodilatory effects directly upon vascular smooth muscle.

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