Results WH (300 M, not its corresponding amino acids) strongly suppressed the increase in [Ca 2 ϩ ] i in angiotensin II (Ang II)-stimulated VSMCs (⌬[Ca 2 ϩ ] i : Control; 620.0 nM, WH; 53.3 nM, P Ͻ 0.01). WH did not attenuate Ang II-induced Ca 2 ϩ release from the endoplasmic/sarcoplasmic reticulum, while signifi cantly inhibited phospholipase C (PLC)activated [Ca 2 ϩ ] i elevation in m-3M3FBS (a PLC activator)-stimulated VSMCs (⌬[Ca 2 ϩ ] i : Control; 221.8 nM, WH; 63.2 nM, P Ͻ 0.01). In PLC-related signaling pathways, involving the facilitation of VDCC by Ca 2 ϩ -related kinases such as CaMK II, WH inhibited CaMK II activity (P Ͻ 0.05). Furthermore, WH suppressed the phosphorylation of VDCC (P Ͻ 0.05).
ConclusionsIn AngII-induced vasoconstriction signaling pathway, we demonstrated for the fi rst time that WH regulates [Ca 2 ϩ ] i in VSMCs through the suppression of PLC/CaMK II/VDCC phosphorylation pathway.
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