PubMed · 2005 · 45 citations · 0 references
MedicinePharmacologyIon Channel BiophysicsMolecular PharmacologyPharmacodynamicsCalcium SignalingCardiovascular PharmacodynamicsIon Channel PharmacologyIon Channel PhysiologyVasodilator TherapyCalcium Channel PharmacologyCalcium Release From Intracellular StoresVasoactive Drug MechanismsVasodilator Pharmacology
The aims of the present study were to investigate the vasoactive effects of luteolin and its mechanisms of action on the rat thoracic aorta. Luteolin (4.5-36 micromol/L) caused a concentration-dependent relaxation of endothelium-intact or endothelium-denuded aortic rings precontracted with phenylephrine (PE, 10(-6) mol/L) or a high level of K+ (6 x 10(-2) mol/L). Luteolin induced a shift of the PE concentration-response curve to the right and downward. L-NAME and propranolol did not influence the vascular effect of luteolin. However, 5-hydroxydecanoate, tetraethylammonium, BaCl2 and 4-aminopyridine significantly attenuated the vasorelaxant effect of luteolin. In Ca2+ -free medium, medium with graded concentrations of Ca2+, or K+ -free solution, luteolin reduced PE-induced contraction. It is concluded that luteolin induces endothelium-independent relaxation in rat thoracic aorta. The mechanism involves the inhibition of sarcolemmal Ca2+ channels, release from intracellular Ca2+ stores and activation of K+ channels.