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Clinics 2011
Gynura procumbens Merr. decreases blood pressure in rats by vasodilatation via inhibition of calcium channelsDOI: 10.1590/S1807-59322011000100025 Keywords: gynura procumbens, hypotension, vasodilatation, calcium channels, butanolic fraction. Abstract: introduction: gynura procumbens has been shown to decrease blood pressure via inhibition of the angiotensinconverting enzyme. however, other mechanisms that may contribute to the hypotensive effect have not been studied. objectives: to investigate the cardiovascular effects of a butanolic fraction of gynura procumbens in rats. methods: anaesthetized rats were given intravenous bolus injections of butanolic fraction at doses of 2.5-20 mg/kg in vivo. the effect of butanolic fraction on vascular reactivity was recorded in isolated rat aortic rings in vitro. results: intravenous administrations of butanolic fraction elicited significant (p<0.001) and dose-dependent decreases in the mean arterial pressure. however, a significant (p<0.05) decrease in the heart rate was observed only at the higher doses (10 and 20 mg/kg). in isolated preparations of rat aortic rings, phenylephrine (1×10-6 m)- or potassium chloride (8×10-2 m)-precontracted endothelium-intact and -denuded tissue; butanolic fraction (1×10-6-1×10-1 g/ml) induced similar concentration-dependent relaxation of the vessels. in the presence of 2.5×10-3 and 5.0×10-3 g/ml butanolic fraction, the contractions induced by phenylephrine (1×10-9-3×10-5 m) and potassium chloride (1×10-2-8×10-2 m) were significantly antagonized. the calcium-induced vasocontractions (1×10-4-1×10-2 m) were antagonized by butanolic fraction concentration-dependently in calcium-free and high potassium (6×10-2 m) medium, as well as in calcium- and potassium-free medium containing 1×10-6 m phenylephrine. however, the contractions induced by noradrenaline (1×10-6 m) and caffeine (4.5×10-2 m) were not affected by butanolic fraction. conclusion: butanolic fraction contains putative hypotensive compounds that appear to inhibit calcium influx via receptor-operated and/or voltage-dependent calcium channels to cause vasodilation and a consequent fall in blood pressure.
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