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 × 10â»6 M)- or potassium chloride (8 × 10⻲ M)-precontracted endothelium-intact and -denuded tissue; butanolic fraction (1 × 10â»6 - 1 × 10⻹ g/ml) induced similar concentration-dependent relaxation of the vessels. In the presence of 2.5 × 10⻳ and 5.0 × 10⻳ g/ml butanolic fraction, the contractions induced by phenylephrine (1 × 10â»9-3 × 10â»5 M) and potassium chloride (1 × 10⻲ - 8 × 10⻲ M) were significantly antagonized. The calcium-induced vasocontractions (1 × 10â»4-1 × 10⻲M) were antagonized by butanolic fraction concentration-dependently in calcium-free and high potassium (6×10⻲ M) medium, as well as in calcium- and potassium-free medium containing 1×10â»6 M phenylephrine. However, the contractions induced by noradrenaline (1 × 10â»6 M) and caffeine (4.5 × 10⻲ 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.
Subject(s)
Asteraceae/chemistry , Blood Pressure/drug effects , Butanols/pharmacology , Plant Extracts/pharmacology , Vasodilation/drug effects , Animals , Calcium/analysis , Calcium Channel Blockers/pharmacology , Heart Rate/drug effects , Male , Plant Leaves , Potassium/analysis , Rats , Rats, Sprague-Dawley , Vasodilator Agents/pharmacologyABSTRACT
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.