Please use this identifier to cite or link to this item: https://scholarbank.nus.edu.sg/handle/10635/133952
Title: Vasorelaxation of rat thoracic aorta caused by 14-deoxyandrographolide
Authors: Zhang, C.Y.
Tan, B.K.H. 
Keywords: 14-Deoxyandrographolide
Aorta
Ca 2+ influx
Nitric oxide
Vasorelaxation
Issue Date: 1998
Citation: Zhang, C.Y., Tan, B.K.H. (1998). Vasorelaxation of rat thoracic aorta caused by 14-deoxyandrographolide. Clinical and Experimental Pharmacology and Physiology 25 (6) : 424-429. ScholarBank@NUS Repository.
Abstract: 1. The pharmacological effects of 14-deoxyandrographolide on rat isolated thoracic aorta were examined. 2. 14-Deoxyandrographolide (2.5-120 μmo/L) inhibited contractions induced by phenylephrine (PE; 0.1 μmol/L) and high K + (80 mmol/L) in a concentration-dependent manner in endothelium- intact aorta. The effect was attenuated in endothelium-denuded aorta without modifying the maximal response. Like verapamil, 14-deoxyandrographolide produced a much greater vasorelaxant effect in aorta precontracted by KCl than by PE. 14-Deoxyandrographolide (20-60 μmol/L) also inhibited responses of the rat aorta to PE. 3. In Ca 2+-free medium (KCl 55 mmol/L), 14- deoxyandrographolide (20-80 μmol/L) antagonized Ca 2+-induced vasocontraction in a concentration-dependent manner and transient contractions induced by both caffeine (10 mmol/L) and noradrenaline (1 μmol/L) were suppressed or almost abolished by 14-deoxyandrographolide. 4. The vasorelaxant effect of 14-deoxyandrographolide was partially antagonized by N(G)-nitro-L-arginine methyl ester (25 μmol/L), a specific and competitive nitric oxide synthase (NOS) inhibitor, and methylene blue (10 μmol/L), a soluble guanylate cyclase inhibitor, but was not affected by indomethacin (20 μmol/L), a cyclo-oxygenase inhibitor, or glibenclamide (10 μmol/L), an ATP-sensitive K +-channel blocker. 5. These results suggest that the vasorelaxant activity of 14-deoxyandrographolide may be mediated via the activation of NOS and guanylate cyclase, as well as the blockade of Ca 2+ influx through both voltage- and receptor-operated Ca 2+ channels.
Source Title: Clinical and Experimental Pharmacology and Physiology
URI: http://scholarbank.nus.edu.sg/handle/10635/133952
ISSN: 03051870
Appears in Collections:Staff Publications

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