Cardiovascular effects of Tacca integrifolia Ker-Gawl. extract in rats

• Main Authors: Prakart Sawangchote, Nongyao Kitjaroennirut, Chaweewan Jansakul
• Format: Article
• Language: English
• Published: Prince of Songkla University 2005-03-01
• Series: Songklanakarin Journal of Science and Technology (SJST)
• Subjects: Tacca integrifolia; blood pressure; vasodilation; nitric oxide; acetylcholine receptors
• Online Access: http://www.sjst.psu.ac.th/journal/27-2-pdf/06Taccaintegrifolia.pdf

Rhizome of Tacca integrifolia, a Thai folk medicinal herb, has been used for controlling blood pressure and improving sexual function in humans. However, the biological activities of this herb on the cardiovascular system have not yet been documented. In the present study, we investigated the cardiovascular effects of methanolic extract from the rhizome of this herb (Tacca extract). In the in vivo study, intravenous injection of the Tacca extract (0.04-40 mg/kg) caused a decrease in both mean arterial blood pressure and heart rate of anesthetized rats (Nembutal sodium, 60 mg/kg, i.p.) in a dose dependent manner. Pretreatment of the animals with muscarinic receptor antagonist, atropine (1 mg/kg, i.v.), significantly reduced the hypotensive and the negative chronotropic activities of the Tacca extract. In the in vitro preparation, the Tacca extract (0.001-3 mg/ml) caused a decrease in both force and rate of spontaneous contraction of isolated atria in a dose dependent manner. These effects were reduced by preincubation of the atria with atropine (10-7 or 10-6 M). For isolated blood vessels, the Tacca extract (0.003-3 mg/ ml) caused vasodilation of endothelium-intact thoracic aortic rings pre-constricted with phenylephrine (3× 10-6 M). This effect disappeared after pre-incubation of blood vessels with atropine (10-6 M) or with Nω-nitro- L-arginine (3×10-4 M), or by removing the vascular endothelium. The results obtained suggest that the hypotensive and negative chronotropic effects of the Tacca extract in the rat are due to the active components acting via the muscarinic receptors at the blood vessel to cause vasodilatation by stimulating the release of nitric oxide, as well as on the muscarinic receptors at the atria to cause the decrease of both rate and force of the atrial contraction.