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Research Article

ScienceAsia 23 (1997): 335-346 |doi: 10.2306/scienceasia1513-1874.1997.23.335



ABSTRACT: Bioassay directed fractionation of the methanolic extract of dried pods and seeds of Moringa oleifera resulted in the isolation of a mixture of thiocarbamate glycosides of niazimicin and niaziminin. In the in vivo preparation, intravenous injection of the compounds (2-16 mg/kg) caused a decrease in mean arterial blood pressure and heart rate of anesthetized rats in dose dependent manner. Pretreatment of the animals with atropine (1.5 mg/kg) did not modify the hypotensive activity or negative chronotropic activity of the compounds. Pre-treatment of the animals with -adrenergic receptor antagonist, DL-propranolol (0.6 mg/kg), caused significant reduction in lowering heart rate activity with no changes in hypotensive activity of the compounds. In the in vitro preparation, the thiocarbamate glycosides (0.02-0.6 mg/ml) caused vasodilatation of thoracic aortic rings pre-constricted with phenylephrine both of endothelium-intact and denuded aortic rings. Pre-incubation of the endothelium-intact aortic rings with NG-nitro-L-arginine (300 mM), a nitric oxide synthase "inhibitor, or with DL-propranolol (10 M), did not abolish the vasodilator activities of the compounds. The thiocarbamate glycosides also caused vasodilatation of the thoracic aortic rings preconstricted with 40 mM KCl. The thiocarbamate glycosides caused a decrease in the rate with no changes on force of contraction of isolated rat atria. Pre-incubation of the atria with the thiocarbamate glycosides (0.6 mg/ml) for 40 min, did not modify the positive chronotropic activity of isoproterenol. It, however, caused significant decreased in force of contraction produced by isoproterenol. These results suggested that the hypotensive and negative chronotropic activity of the thiocarbamate gylcosides are unlikely to be due to the stimulation by the compounds of the muscarinic receptors of the parasympathetic or to their action as a -adrenergic receptor antagonist, but it may act as a Ca2+-channel blocker. However, further studies are needed to clarify this possibility.

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a Department of Physiology, Faculty of Science, Prince of Songkla University, Hat- Yai, Thailand.
b Department of Medicine, The University of Western Australia, Nedland, Australia.
c Department of Organic Chemistry, The University of Western Australia, Nedland, Australia.

Received 7 August 1997