Extracted Anaxagorea luzonensis A. Gray Restored Impairment of Endothelium-Dependent Vasorelaxation Induced by Homocysteine Thiolactone in Rat Aortic Rings.

Objective: To investigate the beneficial effects of Anaxagorea luzonensis (AL) extract on homocysteine thiolactone (HTL)-induced impairment of endothelium-dependent relaxation in rat aortic rings. The mechanisms involved in the effects of AL on endothelial dysfunctions by HTL are also examined.

Material And Method: Aortic rings from male Wistar rats were co-incubated for 90 minutes with L-arginine (3 mM), a precursor of nitric oxide (NO); superoxide dismutase (SOD, 200 U/mL), a scavenger of superoxide anion; indomethacin (10 µM), a cyclooxygenase (COX) inhibitor; SC560 (10 µM), a COX-1 inhibitor; NS398 (10 µM), a COX-2 inhibitor; or SQ29548 (1 µM), a thromboxane A₂ receptor antagonist in the presence of HTL (1 mM).

Mechanisms of vasorelaxation to gamma-mangostin in the rat aorta.

Objective: To investigate the effects of gamma-mangostin on vascular tone and its mechanisms in the isolated rat aorta.

Material And Method: Aortic rings from male Wistar rats were precontracted with methoxamine. Changes in tension were measured using an isometric force transducer and recorded on the MacLab recording system.

Effects of Phikud Navakot extract on vascular reactivity in the isolated rat aorta.

The aim of the present study is to investigate the effect of standardized Phikud Navakot extract (NVKE) on aortic rings from male Sprague Dawley rats. Changes in tension were measured using an isometric force transducer and recorded on the PowerLab recording system. Vasorelaxant effect of NVKE was examined in the presence of indomethacin (10 microM), N(G)-nitro L-arginine methyl ester (L-NAME, 300 microM), methoxamine (0.

Possible mechanisms of vasorelaxation for 5,7-dimethoxyflavone from Kaempferia parviflora in the rat aorta.

The present study investigated the vascular effects of 5,7-dimethoxyflavone (DMF), isolated from the rhizomes of Kaempferia parviflora (KP), on rat isolated aortic rings and its possible mechanisms. DMF (1-100 μM) caused concentration-dependent relaxations in aortic rings precontracted with methoxamine. This effect was significantly reduced by removal of the endothelium, and after pretreatment with N(G)-nitro-L-arginine methyl ester (L-NAME, 300 μM), indomethacin (10 μM) and 1H-[1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one (ODQ, 10 μM), but not 9-(tetrahydro-2-furanyl)-9H-purine-6-amine (SQ22536, 100 μM).

Mechanisms of vasorelaxation to 17beta-oestradiol in rat arteries.

We have investigated the involvement of the endothelium, K+ channels, oestradiol receptors, and Ca2+ influx in 17beta-oestradiol-induced vasorelaxation in rat mesenteric arterial beds and aortae. 17beta-Oestradiol (10 pM-1 mM) caused acute vasorelaxations in mesenteric arterial beds and aortae from male and female rats. In male rat mesenteric vessels and aortae, the vasorelaxations were mostly independent of the endothelium and nitric oxide (NO).

Mechanisms of vasorelaxation to testosterone in the rat aorta.

We have investigated the role of endothelium-derived relaxing factors, K(+) channels and steroid receptors in vasorelaxation to testosterone in the rat aorta. Testosterone (1 nM-mM) caused acute concentration-dependent vasorelaxation. Both indomethacin (10 microM) and flurbiprofen (10 microM) uncovered relaxant responses to testosterone.

Testosterone-induced vasorelaxation in the rat mesenteric arterial bed is mediated predominantly via potassium channels.

We have investigated the involvement of nitric oxide and K(+) channels in the vasorelaxant responses to physiologically-relevant concentrations of testosterone in the rat isolated mesenteric arterial bed. Testosterone (100 pM - 10 microM) elicited concentration-dependent relaxations in the isolated mesenteric arterial bed (pEC(50)=9.47 (9.