These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Endothelium nitric oxide-independent vasorelaxant effects of the aqueous extract from Stephania abyssinica on the isolated rat thoracic aorta.
    Author: Nguelefack TB, Fodem C, Nguelefack-Mbuyo EP, Nyadjeu P, Wansi SL, Watcho P, Kamanyi A.
    Journal: J Complement Integr Med; 2015 Mar; 12(1):15-21. PubMed ID: 25390028.
    Abstract:
    BACKGROUND: Stephania abyssinica (Dillon & A. Rich) Walp (Menispermaceae) is a medicinal plant used in the west region of Cameroon to treat arterial hypertension. The present study evaluated the vasorelaxant effects of the aqueous (AESA) and methanol (MESA) extracts from the fresh leaves of S. abyssinica on aorta rings isolated from Wistar rats. METHODS: Aorta rings with intact endothelium were contracted with KCl (60 mM) or phenylephrine (10-5 M) and exposed to cumulative concentrations of each extract, ranging from 10 to 1,000 µg/mL. The vasorelaxant effects of AESA were further evaluated in presence of Nω-nitro-L-arginine methyl ester (L-NAME, 10-4 M), tetraethylammonium (TEA, 5 µM), glibenclamide (5 µM), propranolol (5 µM), and the association glibenclamide-propranolol (AGP). In another set of experiments, the effect of AESA was evaluated on calcium-induced contraction in a hyperpotassic milieu. RESULTS: AESA and MESA exhibited a concentration-dependent vasorelaxation on KCl-contracted aortic rings with respective EC50 of 160.10 and 346.50 µg/mL. AESA similarly relaxed aortic rings contracted with phenylephrine (EC50, 176.80 µg/mL). The vasorelaxant activity of AESA was not significantly affected by L-NAME but was markedly reduced by TEA, glibenclamide, propranolol, and AGP. AESA strongly inhibited the Ca2+-induced contraction by 95%. CONCLUSIONS: These results support the use of S. abyssinica against arterial hypertension and suggest that the vasorelaxant effect of AESA is not mediated via the endothelium/nitric oxide pathway. AESA relaxant properties might be due to an inhibition of Ca2+ influx and/or the activation of ATP-sensitive K+ channels probably via the stimulation of β-adrenergic receptors.
    [Abstract] [Full Text] [Related] [New Search]