INTRODUCTION:Gynura procumbens has been shown to decrease blood pressure via inhibition of the angiotensin‐converting 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.

BackgroundOleic acid has been shown to lower high blood pressure and provide cardiovascular protection. Curiosity arises as to whether super olein (SO), red palm olein (RPO) and palm olein (PO), which have high oleic acid content, are able to prevent the development of hypertension.Methodology/Principal FindingsFour-week-old male spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats were fed 15% SO, RPO or PO supplemented diet for 15 weeks. After 15 weeks of treatment, the systolic blood pressure (SBP) of SHR treated with SO, RPO and PO were 158.4±5.0 mmHg (p<0.001), 178.9±2.7 mmHg (p<0.001) and 167.7±2.1 mmHg (p<0.001), respectively, compared with SHR controls (220.9±1.5 mmHg). Bradycardia was observed with SO and PO. In contrast, the SBP and heart rate of treated WKY rats were not different from those of WKY controls. The SO and PO significantly reduced the increased heart size and thoracic aortic media thickness observed in untreated SHR but RPO reduced only the latter. No such differences, however, were observed between the treated and untreated WKY rats. Oil Red O enface staining of thoracic-abdominal aorta did not show any lipid deposition in all treated rats. The SO and RPO significantly raised serum alkaline phosphatase levels in the SHR while body weight and renal biochemical indices were unaltered in both strains. Serum lipid profiles of treated SHR and WKY rats were unchanged, with the exception of a significant reduction in LDL-C level and total cholesterol/HDL ratio (atherogenic index) in SO and RPO treated SHR compared with untreated SHR.ConclusionThe SO, RPO and PO attenuate the rise in blood pressure in SHR, accompanied by bradycardia and heart size reduction with SO and PO, and aortic media thickness reduction with SO, RPO and PO. The SO and RPO are antiatherogenic in nature by improving blood lipid profiles in SHR.

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Intravenous injection of the aspidofractinine alkaloid, kopsingine (1, 0.2-10.0 mg/kg) from Kopsia teoi, produced dose-related decreases in the mean arterial blood pressure and heart rate in anesthetized spontaneously hypertensive rats, which were similar to those seen in normotensive controls. Minor modifications in the molecular structure of kopsingine, as in kopsaporine (2, the 12-demethoxy derivative of kopsingine) and 14,15-dihydrokopsingine (4), did not significantly alter the hypotensive responses, whereas a more drastic change in the structure, as in the heptacyclic kopsidine A (3) and the 3-to-17 oxo-bridged compound 5, resulted in an increase in blood pressure. The antihypertensive effects of kopsingine (1) and its congeners (2 and 4) along with the pressor effects produced by the heptacyclic oxo-bridged compounds (5 and 3) could be ascribed to central as well as peripheral actions.

Objectives: To investigate the antihypertensive activity of aqueous extracts obtained from Malaysian coastal seaweeds and to determine the pharmacological mechanisms of the extracts on rat aorta in vitro. Materials and Methods: The antihypertensive activity of 11 species of seaweeds (5 brown, 1 red and 5 green algae) were tested by cumulative addition of the extracts to phenylephrine (PE)-precontracted Wistar-Kyoto (WKY) aortic rings in in vitro isometric contraction studies. Mechanisms for vasorelaxant effect were investigated in the presence of various antagonists. Results: Of the 11 species tested, 2 showed a vasorelaxant effect. Further investigation of the mechanisms of action of the aqueous extract of green alga, Cladophora patentiramea (AECP),showed that the vascular relaxant effect was endothelium- and concentration-dependent. A maximum relaxation of 45.8 ± 4.6% (n = 8, p < 0.001) was obtained at 0.1 mg/ml of extract, after which the response was found to reduce in a concentration-dependent manner to 15.7 ± 4.9% (n = 8, p < 0.001) at the highest extract concentration tested. Pretreatment of endothelium-intact aortic rings with Nω-nitro-L-arginine methyl ester (L-NAME, 30 µM), ¹H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ, 10 µM) and methylene blue (100 µM) resulted in a complete blockade of AECP-induced vasorelaxation. However, the relaxant effects of the extract were not blocked by atropine (1 µM), indomethacin (10 µM) and glibenclamide (10 µM), although the maximum relaxant responses were enhanced in the presence of glibenclamide. Conclusion: Our data showed that the in vitro vascular relaxant effect of AECPwas mediated through endothelium-dependent nitric oxide-cGMP pathway, and was not associated with the release of vasodilator prostaglandins, activation of muscarinic receptors, or ATP-sensitive potassium channels opening.