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Quercetin is one of the most common flavonoids in the human daily diet. Its affects the coronary artery, especially L-type voltage-gated Ca2+ channels and voltage-gated K+ channels in the arterial smooth muscle cells, which are poorly understood. The present experiments were designed to study the myogenic effect of quercetin and its possible underlying mechanisms in the rat coronary artery. A wire myograph was used to observe the myogenic effects. Arterial smooth muscle cells were freshly isolated from the rat coronary artery and the intracellular free Ca2+ concentration was measured with molecular probe fluo-4-AM. The effects of quercetin on L-type voltage-gated Ca2+ channels and voltage-gated K+ channels were studied using a whole-cell patch clamp. Quercetin (3-30 µM) produced a depression and relaxation on the contraction induced by KCl or the thromboxane A2 analog 9,11-Dideoxy-9α,11α-methanoepoxy prostaglandin F 2α . The vasorelaxation was attenuated by 4-aminopyridine, a specific voltage-gated K+ channel inhibitor, but was not affected by the NG-nitro-L-arginine methylester ester (a nitric oxide synthesis inhibitor), glibenclamide (a ATP-activated K+ channel inhibitor), iberiotoxin (a Ca2+-activated K+ channel inhibitor), BaCl2 (an inward rectifier K+ channel inhibitor), or by endothelium denudation. At the same concentrations, quercetin reduced the KCl-induced elevation of the intracellular free Ca2+ concentration, inhibited the inward Ca2+ currents through L-type voltage-gated Ca2+ channels, and increased the outward K+ currents through voltage-gated K+ channels in the rat coronary artery smooth muscle cells. Collectively, our results demonstrate that quercetin possesses vasospasmolytic effects in RCA and suggest that depression of the Ca2+ influx through L-type voltage-gated Ca2+ channels and augmentation of voltage-gated K+ channel activity in the myocytes may underlie coronary relaxation.

The actions and mechanisms of taurine on vascular contractions have been studied in the isolated porcine coronary artery. Taurine depressed histamine-, serotonin-, KCl- and CaCl(2)-induced contractions in a concentration-dependent manner, with maximal contractions being depressed by 43.4%, 46.2%, 33.3% and 43.3%, respectively. Taurine relaxed arterial rings that were precontracted by either 30mM KCl or 0.3 muM U46619, a thromboxane A(2) analog, in a concentration-dependent manner, and the maximal relaxations were 39.4% and 38.7%, respectively. The vasorelaxations were nearly abolished by pretreatment with either the inward rectifier K(+) channel (K(IR)) inhibitor, BaCl(2), or the ATP sensitive K(+) channel (K(ATP)) inhibitor, glibenclamide, and were attenuated by the Ca(2+)-activated K(+) channel (K(Ca)) inhibitor tetraethylammonium. Denudation of the endothelium, and treatment with the nitric oxide synthase inhibitor, L-NAME, the cyclooxygenase inhibitor, indomethacin, or the voltage gated K(+) channel (K(V)) inhibitor 4-aminopyridine did not affect the relaxation. The present results show that taurine antagonizes and relaxes the contractions of the porcine coronary artery, and suggest that the activation of K(IR), K(ATP) and K(Ca) may be involved in taurine-induced relaxation of the porcine coronary artery.

Nebivolol produced a concentration-dependent vasodilation in different rat arteries precontracted by PE or KCl. In the isolated rat aorta, carotid artery, femoral artery, and renal artery, neither K(+) channels nor PI3K/Akt pathway was involved in the relaxation induced by nebivolol.