The aim of the present study was to investigate the mechanisms by which Hibiscus sabdarifa petal extract produces its well-established antihypertensive activity, from both pharmacological and biochemical aspects of view. Pharmacologically, the aqueous extract exhibited a hypotensive effect when injected intravenously (femoral vein) in anesthetized rats cannulised via femoral artery and connected to pressure transducer. This hypotensive effect was resistant to prior administration of different pharmacological blockers, including atropine (0.2 mg/250 g. b. wt.), hexamethonium (2 mg/250 g. b. wt.), propranolol (0.1 mg/250 g. b. wt.) and phentolamine (0.1 mg/250 g. b. wt.). The aqueous extract showed concentration-dependent relaxation of noradrenaline-precontracted aortic rings using tension recording technique. This relaxation was resistant to tetrodotoxin (neuronal blocker; 0.25 μM), L-NAME (Nitric oxide synthase inhibitor; 200 μM), indomethacin (cyclo-oxygenase inhibitor; 10 μM) nifedipine (Ca++ channel blocker; 10 μM), apamin (small conductance K+ channel blocker; 1 μM), glibenclamide (ATP-sensitive K+ channel blocker; 100 μM) and endothelial denudation. Biochemically, the aqueous extract of Hibiscus petals exhibited significant decrease in serum levels of ACE, total cholesterol, tri-acylglycerols, LDL and VLDL as well as Na+ concentration in hyperlipidemic rats; but raised the level of HDL; with no significant effect on serum K+. The obtained results may indicate that Hibiscus petal extract produces its antihypertensive action via four mechanisms; first is direct relaxing the vascular smooth muscle; the second is decreasing the level of ACE in serum; the third is decreasing the elevated blood lipid profile; while and the fourth is decreasing serum Na+ level. |
