Abstract

Objective: This study aimed to investigate the effects of Ficus deltoidea leaves methanolic and water extracts on the vascular reactivity compared with losartan, particularly on the contribution of endothelium-derived relaxing factor, nitric oxide (NO), prostacyclin, and the angiotensin receptor type 1 (AT1) in spontaneously hypertensive rats (SHRs). Method: SHRs (230-280 g) were divided into 4 groups: control (SHRN), losartan (10 mg/kg body weight)(SHRP), Ficus deltoidea methanolic extracts (1 g/kg BW)(SHRM) and Ficus deltoidea water extracts (1 g/kg BW)(SHRW). All groups received daily oral treatment for 14 days. Isolated endothelium intact and denuded thoracic aortic rings were used and subjected to endothelium-dependent and independent contraction studies using phenylephrine (PE) (10-9 to 10-5mol/l). Isolated endothelium intact thoracic aortic rings were harvested and subjected to endothelium-dependent relaxation of acethylcholine (ACh) (10-9 to 10-5mol/l) in the absence and presence of 100 μM Nω-nitro-L-arginine methyl ester (L-NAME) and 10 μM indomethacin. Results: SHRP and SHRW groups reduced significantly vasoconstriction responses to PE in intact aortic rings when compared to denuded. Both SHRN and SHRM groups showed significantly greater tension after removal of endothelium. All groups showed significantly greater relaxation to ACh when compared to SHRN. Inhibition of NO synthesis with L-NAME showed significantly impaired endothelium-dependent relaxation in all groups. However, inhibition of cyclooxygenase (COX) pathway by indomethacin had significantly impaired endothelium-dependent relaxation in SHRP and SHRM groups only. Conclusion: Collectively, these findings suggest that both Ficus deltoidea water and methanolic extracts possess antihypertensive effects but acting on different mechanisms in SHRs. Ficus deltoidea water extract involves endothelium-derived NO but not the prostacyclin pathway, whereas the methanolic extract involves NO/COX pathway. Inhibition of the synergistic activity between AT1 receptor and α1-adrenergic receptor may also possible.

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