BackgroundMorinda citrifolia (Noni) is an edible plant with wide range of medicinal uses. It occurs exclusively in tropical climate zone from India through Southeast Asia and Australia to Eastern Polynesia and Hawaii. The objective of this study was to explore the possible mode(s) of action for its antispasmodic, vasodilator and cardio-suppressant effects to rationalize its medicinal use in gut and cardiovascular disorders.MethodsIsolated tissue preparations such as, rabbit jejunum, rat and rabbit aorta and guinea pig atria were used to test the antispasmodic and cardiovascular relaxant effects and the possible mode of action(s) of the 70% aqueous-ethanolic extract of Morinda citrifolia roots (Mc.Cr).ResultsThe Mc.Cr produced a concentration-dependent relaxation of spontaneous and high K+ induced contractions in isolated rabbit jejunum preparations. It also caused right ward shift in the concentration response curves of Ca++, similar to that of verapamil. In guinea-pig right atria, Mc.Cr caused inhibition of both atrial force and rate of spontaneous contractions. In rabbit thoracic aortic preparations, Mc.Cr also suppressed contractions induced by phenylephrine (1.0 μM) in normal- Ca++ and Ca++-free Kerb's solutions and by high K+, similar to that of verapamil. In rat thoracic aortic preparations, Mc.Cr also relaxed the phenylephrine (1.0 μM)-induced contractions. The vasodilatory responses were not altered in the presence of L-NAME (0.1 mM) or atropine (1.0 μM) and removal of endothelium.ConclusionsThese results suggest that the spasmolytic and vasodilator effects of Mc.Cr root extract are mediated possibly through blockade of voltage-dependent calcium channels and release of intracellular calcium, which may explain the medicinal use of Morinda citrifolia in diarrhea and hypertension. However, more detailed studies are required to assess the safety and efficacy of this plant.
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.
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