| Summary: | 碩士 === 大仁科技大學 === 製藥科技研究所 === 98 === The present study was to evaluate the cardiovascular activity of the essential oil of Cymbopogon citratus (EOCC) and its main constituent citral, and to explore the possible mechanism of action in isolated rat aorta and spontaneously hypertensive rats (SHR, 300-350 g). In isolated rat aortic rings pre-contracted with KCl (60 mM), EOCC (1-100 ×10-5 v/v) and citral (1-100 ×10-5 v/v) provoked a potent vasorelaxant effect in a concentration-dependent manner. This EOCC and citral-induced aortic relaxation was markedly inhibited by pretreatment with an Ca2+-activated K+ channel blocker, tetraethylammonium chloride (TEA, 1mM), but not by endothelium removal or nitric oxide (NO) synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME, 100 µM). In SHR with established hypertension, EOCC (5–30 mg/kg, i.v.) elicited biphasic dose-dependent antihypertensive and cardiac inhibitory effects, whereas citral (1-20 mg/kg) produced only immediate but transient vasodepressor effects. These EOCC or citral responses were greater in SHR than normotensive rats. The EOCC and citral-induced initial antihypertensive effects were significantly blocked by pretreatment with TEA (4 mg/kg, i.v.) and hexamethonium (HEX, 30 mg/kg, i.v.), whereas the delayed effects of EOCC were reversed by pretreatment with L-NAME (20 mg/kg, i.v.) and HEX (30 mg/kg, i.v.) and 4-aminopyridine (4AP, 0.2 mg/kg, i.v.). These results demonstrate for the first time that the EOCC exerts a transient followed by a delayed antihypertensive and cardiac inhibitory effects, whereas citral produced only transient antihypertensive and cardiac inhibitory effects . We further revealed that initial antihypertensive effect elicited by EOCC and its main constituent citral may through direct endothelium-independent vascular relaxation associated with activation of opening Ca2+-activated K+ channel as well as the withdrawal of sympathetic, whilst activation of nitric oxide signals pathway and valtage-sensitive potassium channels, and sympathetic inhibition may contribute to delayed effect of EOCC.
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