Proceedings of The Physiological Society

Physiology 2014 (London, UK) (2014) Proc Physiol Soc 31, PCB190

Poster Communications

Potassium channels contribute to vasorelaxant activities induced by Tridax procumbens aqueous leave extract in rat mesenteric artery

H. M. Salahdeen2,1, A. A. Alada1,2, B. A. Murtala1,2, A. O. Adebari2,1

1. Physiology, Lagos State University College of Medicine, Lagos, Ikeja, Nigeria. 2. Physiology, University of Ibadan, Ibadan, Ibadan, Nigeria.


  • Fig 1: Concentration response curves for T. procumbens in mesenteric artery precontracted with PE (10-6 M) filled circle and KCl (60mM) open circle. Each point represents mean

  • Fig 2: Concentration response curves for T. procumbens extract in mesenteric artery precontracted with PE (10-6 M) in present of L-NAME (10-4M) and indomethacin (10-4M). Each point represents mean

AbstractPrevious studies of Tridax procumbens have shown that aqueous leaves extract are capable of lowering the blood pressure of rats through endothelium-dependent and -independent mechanisms in aortic rings isolated from rats. In the present study, we further investigated Tridax procumbens-induced relaxation in rat isolated mesenteric artery, assessing its interaction with nitric oxide (NO) synthase and K+ channels inhibitors. The in vitro effect of T. procumbens extract on vascular tension was studied using isolated rat mesenteric artery. The effects of the extract on potassium (K+) channels, NOsynthase inhibitor, prostacyclin productions and guanylyl cyclase activities were also examined. The T. procumbens extract ranging from (0.5 - 9mg/ml) significantly (p<0.05) inhibited and sustained tonic contraction induced by phenylephrine and potassium chloride in a concentration-dependent manner. The extract also antagonised the calcium-induced vasoconstrictions (10-9-10-5M) in calcium-free with high concentration of potassium as well as in calcium- and potassium free Krebs-Henseleit solutions. The vasorelaxing effect caused by T. procumbens extract was significantly (p<0.05) attenuated with preincubation of potassium channels blockers (Barium chloride and apamin) NO synthase inhibitor (L-NAME), prostacyclin inhibitor (indomethacin), atropine, and methylene blue while it was not affected by preincubation with glibenclamide and tetraethlammnium, oxadiazolo quinaoxalinone and propanolol. The results demonstrate that T. procumbens causes vasodilatory effects by blocking calcium channels, stimulation of prostacyclin production and activation of both voltage- (KV) and apamin-sensitive (KAS) potassium channels.

Where applicable, experiments conform with Society ethical requirements