Abstract
Trp‐His is the only vasoactive di‐peptide known to regulate intracellular Ca2+([Ca2+]i) and prevent the onset of atherosclerosis in mice. In this study, we showed that Trp‐His reduced the [Ca2+]ielevation in phospholipase C‐activated vascular smooth muscle cells (VSMCs), while a mixture of the corresponding constituent amino acids did not show significant reduction. Furthermore, Trp‐His suppressed calmodulin‐dependent kinase II (CaMK II) activity in angiotensin II‐stimulated VSMCs, resulting in the inhibition of phosphorylation of voltage‐dependent L‐type Ca2+channels (VDCC). Therefore, Trp‐His potentially regulates the VDCC phosphorylation cascade through Ca2+‐CaM/CaMK II.