Cardiovascular effects of the
essential oil of Croton zehntneri (EOCZ) were investigated in conscious rats. In these preparations, intravenous (i.v.)
injections of EOCZ (1-20 mg kg(-1)) and its main constituents
anethole and
estragole (both at 1-10 mg kg(-1)) elicited brief and dose-dependent
hypotension and
bradycardia (phase I) that were followed by a significant pressor effect associated with a delayed
bradycardia (phase II). The initial
hypotension and
bradycardia (phase I) of EOCZ were unchanged by
atenolol (1.5 mg kg(-1), i.v.) or
L-NAME (20 mg kg(-1), i.v.) pretreatment, but were respectively reversed into pressor and tachycardic effects by
methylatropine (1 mg kg(-1), i.v.) pretreatment. The subsequent pressor effect and the delayed
bradycardia (phase II) remained unaffected by
atenolol, but were abolished by
L-NAME and
methylatropine pretreatment, respectively. In rat endothelium-containing aorta preparations, the
vasoconstrictor responses to
phenylephrine were enhanced and reduced, respectively, by the lower (1-30 microg mL(-1)) and higher (300-1000 microg mL(-1)) concentrations of EOCZ. Only the enhancement of
phenylephrine-induced contraction was abolished by either the incubation with
L-NAME (50 microM) or in the absence of the endothelium. These data show, for the first time, that i.v. administration EOCZ induces an initial
hypotension followed by a pressor response, two effects that appear mainly attributed to the actions of
anethole and
estragole. The EOCZ-
induced hypotension (phase I) is mediated by a
cholinergic mechanism and seems to result mainly from the concomitant
bradycardia. The pressor response of EOCZ (phase II) seems to be caused by an indirect vasoconstrictive action of EOCZ most likely through inhibition of endothelial
nitric oxide production.