Extract Restores Smooth Muscle Vasorelaxation in Rat Carotid Arteries Even under High Extracellular K Concentrations.

Recent studies showed that (CL) has antihypertensive effects. However, to date, no study has examined the effects of CL on vascular tone under a high extracellular K concentration ([K]). Thus, the present study examined the effect of an extract of (ECL) on the vascular tension of rat carotid arteries exposed to high [K]. We used myography to investigate the effect of an ECL on the vascular tension of rat carotid arteries exposed to high [K] and the underlying mechanism of action. In arteries with intact endothelia, the ECL (250 μg/mL) had no effect on vascular tension in arteries exposed to normal or high [K]. In contrast, the ECL significantly increased vasorelaxation in endothelium-impaired arteries exposed to a physiologically normal or high [K] compared with control arteries exposed to the same [K] conditions in the absence of ECL. This vasorelaxing action was unaffected by a broad-spectrum K channel blocker and an ATP-sensitive K channel blocker. The ECL significantly inhibited the vasoconstriction induced by Ca influx through voltage-dependent Ca channels (VDCCs) but not Ca influx induced via receptor-operated Ca channels or the release of Ca from the sarcoplasmic reticulum in the vascular smooth muscle. In summary, our study reveals that the ECL acts through VDCCs in vascular smooth muscle to promote the recovery of vasorelaxation even in arteries exposed to high [K] in the context of endothelial dysfunction and provides further evidence of the vascular-protective effects of ECL.