Cardiovascular effects of the
essential oil of Croton argyrophylloides Muell. Arg. (EOCA) were investigated in normotensive rats. In saline-pretreated anesthetized or conscious rats, intravenous (i.v.) injection of the EOCA induced dose-dependent
hypotension. Dose-dependent
tachycardia was observed only in conscious rats. In anesthetized rats, cervical bivagotomy failed to enhance EOCA-
induced hypotension but unmasked significant
bradycardia. In conscious rats, i.v. pretreatment with
methylatropine, but not with
atenolol or
L-NAME, reduced both hypotensive and tachycardiac responses to EOCA. However,
hexamethonium pretreatment reverted the EOCA-induced
tachycardia into significant
bradycardia without affecting the
hypotension. In aortic ring preparations precontracted with
phenylephrine, EOCA induced a concentration-dependent relaxation that was significantly reduced by vascular endothelium removal and pretreatment with
atropine,
indomethacin, or
glibenclamide but remained unaffected by pretreatment with
L-NAME or
TEA. It is concluded that i.v. treatment with EOAC decreased blood pressure probably through an active vascular relaxation rather than withdrawal of sympathetic tone.
Muscarinic receptor stimulation, liberation of the endothelium-derived
prostacyclin, and opening
KATP channels are partially involved in the aortic relaxation induced by EOCA and in turn in the mediation of EOCA-
induced hypotension. EOCA-induced
tachycardia in conscious rats appears to be mediated reflexly through inhibition of vagal drive to the heart.