Farrerol, isolated from Rhododendron dauricum L., has been proven to be an important multifunctional physiologically active component, but its vasoactive mechanism is not clear. The present study was performed to observe the vasoactive effects of farrerol on rat aorta and to investigate the possible underlying mechanisms. Isolated aortic rings of rat were mounted in an organ bath system and the myogenic effects stimulated by farrerol were studied. Intracellular Ca²⁺ ([Ca²⁺]_in) was measured by molecular probe fluo-4-AM and the activities of L-type voltage-gated Ca²⁺ channels (LVGC) were studied with whole-cell patch clamp in cultured vascular smooth muscle cells (VSMCs). The results showed that farrerol significantly induced dose-dependent relaxation on aortic rings, while this vasorelaxation was not affected by N^G-nitro-l-arginine methylester ester or endothelium denudation. In endothelium-denuded aortas, farrerol also reduced Ca²⁺-induced contraction on the basis of the stable contraction induced by KCl or phenylephrine (PE) in Ca²⁺-free solution. Moreover, after incubation with verapamil, farrerol can induce relaxation in endothelium-denuded aortas precontracted by PE, and this effect can be enhanced by ruthenium red, but not by heparin. With laser scanning confocal microscopy method, the farrerol-induced decline of [Ca²⁺]_in in cultured VSMCs was observed. Furthermore, we found that farrerol could suppress Ca²⁺ influx via LVGC by patch clamp technology. These findings suggested that farrerol can regulate the vascular tension and could be developed as a practicable vasorelaxation drug.

The vasodilator effect of apigenin (API) was demonstrated in a number of vascular beds. We aimed to characterize the vasospasmolytic and electrophysiological effects of apigenin (API) in intrarenal arteries (IRAs). The vascular tone of male rat isolated IRAs was recorded with a myograph. Transmembrane Cl ⁻ currents through Ca ²⁺ -activated Cl ⁻ channels (CaCCs), K ⁺ currents through voltage-gated K ⁺ (Kv) channels and inwardly rectifier K ⁺ (Kir) channels were recorded with patch clamp in the freshly isolated arterial smooth muscle cells (ASMCs). Preincubation with API (10-100 μM) concentration-dependently depressed the contractions induced by KCl, 9,11-dideoxy-9α,11α-methanoepoxy prostaglandin F _2α (U46619), phenylephrine and vasopressin without significant preference and the IC ₅₀ values were 13.27-26.26 μM. Acute application of API elicited instant relaxations in the IRAs precontracted with these vasoconstrictors and the RC ₅₀ values were 5.80-24.33 μM. API relaxation was attenuated by chloride deprivation, CaCC blockers, Kv blocker and nitric oxide synthase inhibitor, but not by Kir blocker and cyclooxygenase inhibitor. At 10-100 μM, API depressed CaCC currents and Kir currents while enhanced Kv currents of IRA ASMCs. The present results demonstrate that API counteracts various vasoconstrictors noncompetitively and nonspecifically and suggest that modulation of CaCCs, Kv and Kir channels of IRA ASMCs is involved in its vasospasmolytic effects.