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BackgroundThis study was undertaken to provide pharmacological basis for the medicinal use of Viola odorata Linn. in hypertension and dyslipidemia using the in vivo and in vitro assays.ResultsViola odorata leaves extract (Vo.Cr), which tested positive for alkaloids, saponins, tannins, phenolics, coumarins and flavonoids, caused a dose-dependent (0.1-1.0 mg/kg) decrease in mean arterial blood pressure in anaesthetized rats. In isolated guinea-pig atria, Vo.Cr equally inhibited force and rate of spontaneous atrial contractions. On the baseline of rat thoracic aortae (endothelium-intact and denuded), the plant extract caused phentolamine-sensitive vasoconstriction. When tested on phenylephrine (PE, 1 μM) and K+ (80 mM)-induced vasoconstriction, Vo.Cr caused a concentration-dependent relaxation and also caused a rightward shift of Ca++ concentration-response curves as well as suppression of PE (1 μM) control peaks in Ca++-free medium, similar to that caused by verapamil. In the presence of L-NAME, the relaxation curve of Vo.Cr was partially inhibited showing involvement of Nitric oxide (NO) mediated pathway. In Tyloxapol-induced dyslipidemia, Vo.Cr caused reduction in total cholesterol and triglyceride levels. In high-fat diet-induced dyslipidemia model, the plant extract caused a significant decrease in total cholesterol, LDL-C, atherogenic index and prevented the increase in average body weights, while it increased HDL-C.ConclusionsThese data indicate that the vasodilator effect of the plant extract is mediated through multiple pathways like inhibition of Ca++ influx via membranous Ca++ channels, its release from intracellular stores and NO-mediated pathways, which possibly explain the fall in BP. The plant also showed reduction in body weight and antidyslipidemic effect which may be due to the inhibition of synthesis and absorption of lipids and antioxidant activities. Thus, this study provides a pharmacologic rationale to the medicinal use of Viola odorata in hypertension and dyslipidemia.

The objective of this study was to investigate the possible mode(s) of action for the medicinal use of Orchis mascula (OM) (family Orchidaceae) in hypertension and dyslipidemia. In spontaneously hypertensive rats (SHRs), OM significantly (Po0.05) reduced systolic blood pressure to 174.2±9.63 vs. 203.4±7.13 mm Hg (mean±s.e.m.; n¼7-10) and improved endothelial dysfunction by increasing acetylcholine-induced relaxation. In normotensive anesthetized rats, the crude extract of OM (Om.Cr) at 10 and 30 mg kg À1 caused a dose-dependent attenuation of mean arterial pressure. OM also decreased serum triglycerides to 29.28 ± 6.99 vs. 93.84 ± 5.7 mg per 100 ml (Po0.001), low-density lipoprotein-cholesterol to 5.99 ± 1.27 vs. 21.9 ± 3.5 mg per 100 ml (Po0.05) and atherogenic index to 0.096±0.017 vs. 0.36±0.08 mg per 100 ml (Po0.05). OM significantly reduced lipid levels in tyloxapol and high fat diet-induced hyperlipidemia. In a second model, OM also reduced gain in body weight with a reduction in daily diet consumption. In isolated rabbit aorta, Om.Cr caused concentration-dependent relaxation of both phenylephrine and high K + (80 mM)-induced contractions and a rightward shift of the calcium concentration-response curves similar to the effect seen with verapamil. In conclusion, OM shows antihypertensive and endothelial-modulating effects mediated through multiple pathways that include direct vasodilation by calcium channel blockade and reduction of plasma lipids by inhibition of biosynthesis, absorption and secretion. This study rationalizes the medicinal use of OM in hypertension and dyslipidemia. However, further studies are required to identify the active constituents of this plant.