Recent studies showed that Codonopsis lanceolata (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+]o). Thus, the present study examined the effect of an extract of Codonopsis lanceolata (ECL) on the vascular tension of rat carotid arteries exposed to high [K+]o. We used myography to investigate the effect of an ECL on the vascular tension of rat carotid arteries exposed to high [K+]o 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+]o. In contrast, the ECL significantly increased vasorelaxation in endothelium-impaired arteries exposed to a physiologically normal or high [K+]o compared with control arteries exposed to the same [K+]o 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 Ca2+ influx through voltage-dependent Ca2+ channels (VDCCs) but not Ca2+ influx induced via receptor-operated Ca2+ channels or the release of Ca2+ 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+]o in the context of endothelial dysfunction and provides further evidence of the vascular-protective effects of ECL.
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