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Background: Tridax procumbens leaf extract has been reported to show antihypertensive actions through its vasodilatory effects. Although several mechanisms of action have been reported, the sub-cellular mechanism of action of the extract is yet to be fully elucidated. Aim and Objectives: In this study, we investigate the involvement of Na+ - K+ -pump and Na+- Ca2+ exchanger in the vasorelaxant activities of T. procumbens extract (TPE) in isolated rat superior mesenteric arteries. Materials and Methods: Superior mesenteric artery isolated from healthy, young adult Wistar rats (250–300 g) and pre-contracted with phenylephrine (PE) (10-7M) were treated with various concentrations of aqueous extract of TPE (0.5–9 mg/mL). The changes in arterial tension were recorded and interaction between TPE with the selective blocker of Na+ - K+ ATPase (ouabain) and putative Na+-Ca2+ exchanger inhibitor (NiCl2) was evaluated. Results: The result indicated that TPE significantly inhibit the cumulative concentration response curves to PE (10-9 - 10-5 M) in a concentration-dependent manner. Pre-treatment with both ouabain and nickel chloride (NiCl2), abolished the vasorelaxant responses of TPE. Furthermore, TPE reduced the relaxant effect with decreased extracellular Na+ concentration. TPE-induced vasorelaxation was completely abolished in a Na+ -free solution, a condition that eliminates the influence of the forward mode of the exchanger. Conclusion: The results provide direct hypothetical evidence that the activation of Na+ - K+ ATPase and stimulation of the forward mode of the Na+-Ca2+ exchanger contribute to the vasorelaxation induced by TPE in mesenteric artery.

Background/Aim: Tridax procumbens (Linn) (Asteraceae) is one of the herbs widely distributed in many parts of the world. Its leaves have long been used for the treatment of hypertension in Nigeria. Previous studies have shown that aqueous leaves of T. procumbens extract (TPE) lowers blood pressure through endothelium-dependent and -independent mechanism in the aortic rings isolated from normotensive rats. The aim of the present study was to further investigate mechanisms of TPE-induced relaxation in the aortic artery by assessing its mechanistic interactions with nitric oxide (NO) synthase, cyclic guanosine monophosphate (cGMP), and cyclic adenosine monophosphate (cAMP). Materials and Methods: The aortic artery isolated from healthy, young adult normotensive Wistar albino rats (250-300 g) were pre-contracted with phenylephrine (PE) (10–7 M) and KCl (60 mM) and were treated with various concentrations of aqueous extract of TPE (0.5-9.0 mg/ml). The changes in arterial tension were recorded using Ugo Basile model 7004 coupled to data capsule acquisition system model 17400. The interaction between TPE with cAMP and cGMP inhibitors was also evaluated. Results: The results showed that the TPE (0.5-9.0 mg/ml) significantly (P < 0.05) reduced the contraction induced by PE in a concentration-dependent manner. The vasorelaxant effect caused by the TPE was significantly (P < 0.05) attenuated with pre-incubation of cGMP (Rp-8Br PET cGMPS) and cAMP (Rp-AMP) inhibitor, respectively. Conclusion: These results suggest that TPE causes vasodilatory effects in a concentration-dependent manner in the isolated rat aortic artery. The mechanism of action of TPE is complex. A part of its relaxing effect is mediated directly by blocking or modulating cGMP and cAMP.