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Open Access Open Badges Research article

Hypotensive effect of Gentiana floribunda is mediated through Ca++ antagonism pathway

Arif-ullah Khan12*, Mohamad Rais Mustafa1, Asif Ullah Khan3 and Dharmani Devi Murugan1

Author affiliations

1 Centre for Natural Products Research and Drug Discovery, Department of Pharmacology, Faculty of Medicine, University of Malaya, Kuala Lumpur 50603, Malaysia

2 Department of Pharmacy, Kohat University of Science and Technology, Kohat 26000, KPK, Pakistan

3 Institute of Basic Medical Sciences, Khyber Medical University, Peshawar, Pakistan

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Citation and License

BMC Complementary and Alternative Medicine 2012, 12:121  doi:10.1186/1472-6882-12-121

Published: 11 August 2012



Gentiana floribunda was investigated for the possible hypotensive and vasodilator activities in an attempt to rationalize its traditional use in hypertension.


The crude extract of Gentiana floribunda (Gf.Cr) was studied in anaesthetized rats and isolated thoracic aorta tissues.


Gf.Cr which tested positive for presence of flavonoids, saponins, sterols, tannins and terpenes caused dose-dependent (3.0-100 mg/kg) fall in arterial blood pressure (BP) of rats under anaesthesia. In rat aortic ring preparations denuded of endothelium, Gf.Cr at concentration range of 1.0-10 mg/mL relaxed high K+ (80 mM) and phenylephrine (PE, 1 μM)-induced contractions and shifted Ca++ dose–response curves to right, similar to that caused by verapamil. It also suppressed PE (1 μM) control peak responses at 0.3-1.0 mg/mL, obtained in Ca++-free medium, as exhibited by verapamil. Pre-treatment of tissues with Gf.Cr produced rightward non-parallel shift of PE-curves with decline of maximum contractile response. The vasodilator effect of Gf.Cr was endothelial-independent, as it was not blocked by Nω-nitro-L-arginine methyl ester hydrochloride, atropine and indomethacin in endothelium-intact aortic tissues.


These data indicate that BP-lowering action of Gentiana floribunda occurred via Ca++ antagonism (inhibition of Ca++ ingress and release from intracellular stores), which provides pharmacological basis to justify its effectiveness in hypertension.