Emodin activates BK channel in vascular smooth muscle cells and relaxes the interlobar renal artery of rat

Aim: The purpose of this study was to investigate the mechanical and electrophysiological effects of emodin on BK channels in the IRASMCs, of the rat. Methods: Isolated interlobar renal artery was used for vascular reactivity measurements using a pressure myo-graph system. Electrophysiological measurements of single vascular smooth muscle cells were conducted using whole-cell and cell-attached patch-clamp recording. Laser scanning confocal microscope technology was used to measure cytosolic calcium ion signals. Key results: Emodin relaxed the interlobar renal artery and enhanced the outward currents amplitude of IRASMCs in a concentration-dependent manner, and IbTX inhibited these emodin-induced outward currents. Incubation of IRASMCs in a calcium ion free medium for 30 min decreased the observed effects of emodin on IRASMCs membrane currents. Furthermore, the application of nimodipine, an L-Type calcium ion channel blocker, ryanodine, a ryanodine receptor modifier, and heparin, an IP3 receptor blocker, decreased the emodin-induced BK channel currents, respectively. BAPTA-AM, a selective calcium ion chelator, abolished the emodin-induced BK channel currents. Emodin repolarized cytomembrane and enhanced BK channel open probabilities and elevated cytosolic calcium ion concentration. Conclusion: The vasorelaxant effect of emodin on vessels is mediated through the activation of BK channels.

Automated summary

The study aimed to investigate the mechanical and electrophysiological effects of emodin on BK channels in rat interlobar renal artery smooth muscle cells (IRASMCs). The results showed that emodin induced vasorelaxation and enhanced outward currents in a concentration-dependent manner. These effects were mediated through the activation of BK channels.