4.7 Article

Antihypertensive and vasorelaxant effects of tilianin isolated from Agastache mexicana are mediated by NO/cGMP pathway and potassium channel opening

期刊

BIOCHEMICAL PHARMACOLOGY
卷 78, 期 1, 页码 54-61

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PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.bcp.2009.03.016

关键词

Agastache mexicana; Antihypertensive; Nitric oxide; cGMP; Tilianin

资金

  1. CONACyT [89521]

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Current investigation was undertaken to elucidate the mode of action of tilianin, isolated from Agastache mexicana, as a vasorelaxant agent on in vitro functional rat thoracic aorta test and to investigate the in vivo anti hypertensive effect on spontaneously hypertensive rats (SHR). Tilianin (0.002-933 mu M) induced significant relaxation in a concentration- and endothelium-dependent and -independent manners in aortic rings pre-contracted with noradrenaline (NA, 0.1 mu M), and serotonin (5-HT, 100 mu M). Effect was more significant (p < 0.05) in endothelium-intact (+E) aorta rings than when endothelium was removed (-E). Pre-treatment with N-nitro-L-arginine methyl ester (L-NAME; 10 mu M) or 1-H-[1,2,4]-oxadiazolo-[4,3a]-quinoxalin-1-one (ODQ, 1 mu M) produced a significant change of the relaxant response and activity was markedly inhibited, but not by indomethacin (10 mu M) or atropine (1 mu M). Furthermore, tilianin (130 mu M) provoked a significant displacement to the left in the relaxation curve induced by sodium nitroprusside (SNP; 0.32 nM to 0.1 mu M). Moreover, tilianin induced significant in vitro NO overproduction (1.49 +/- 0.86 mu M of nitrites/g of tissue) in rat aorta compared with vehicle (p < 0.05). In addition, pre-treatment with tetraethylammonium (TEA, 5 mM) and 2-aminopyridine (2-AP, 0.1 mu M) shifted to the right the relaxant curve induced by tilianin (p < 0.05). Finally, a single oral administration of tilianin (50 mg/kg) exhibited a significant decrease in systolic and diastolic blood pressures (p < 0.05) in SHR model. Results indicate that tilianin mediates relaxation mainly by an endothelium-dependent manner, probably due to NO release, and also through an endothelium-independent pathway by opening K+ channels, both causing the anti hypertensive effect. (c) 2009 Elsevier Inc. All rights reserved.

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