Cardiovascular effects of ginger aqueous extract and its phenolic constituents are mediated through multiple pathways
Biological and Biomedical Sciences
Ginger is a world known food plant which is equally reputed for its medicinal properties. We report here the hypotensive, endothelium-dependent and independent vasodilator and cardio-suppressant and stimulant effects of its aqueous extract (Zo.Cr). Zo.Cr, which tested positive for saponins, flavonoids, amines, alkaloids and terpenoids, induced a dose-dependent (3.0-10.0 mg/kg) fall in the arterial blood pressure (BP) of anaesthetized rats which was partially blocked by atropine (1 mg/kg). In isolated endothelium-intact rat aorta, Zo.Cr (0.01-5.0 mg/ml) relaxed the phenylephrine (1 microM)-induced contractions, effect partially blocked by atropine (1 microM). Zo.Cr inhibited the K+ (80 mM)-induced contractions and also shifted the Ca++ dose-response curves to the right, similar to verapamil, indicating Ca++ antagonist activity. An atropine-resistant and l-NAME-sensitive vasodilator activity was also noted from ginger phenolic constituents 6-, 8- and 10-gingerol, while 6-shogaol showed a mild vasodilator effect. In guinea-pig atria, Zo.Cr (0.1-5.0 mg/ml) inhibited the force and rate of atrial contractions. Pretreatment with atropine blocked the inhibitory effect and a stimulatory effect was unmasked which was resistant to propranolol and verapamil but sensitive to ryanodine, blocker of Ca++ release from intracellular stores. Later at doses >or=1.0 mg/ml, the extract completely suppressed the atrial tissue, effect resistant to glibenclamide, pyrilamine, aminophylline and L-NAME. These data indicate that the aqueous ginger extract lowers BP through a dual inhibitory effect mediated via stimulation of muscarinic receptors and blockade of Ca++ channels and this study provides sound mechanistic basis for the use of ginger in hypertension and palpitations.
Ghayur, M. N.,
Gilani, A. H.,
Afridi, M. B.,
Houghton, P. J.
(2005). Cardiovascular effects of ginger aqueous extract and its phenolic constituents are mediated through multiple pathways. Vascular Pharmacology, 43(4), 234-241.
Available at: https://ecommons.aku.edu/pakistan_fhs_mc_bbs/429