Vascular smooth muscle cells feature L-type voltage-gated calcium channels in their plasma membrane. Upon depolarization, these channels open, and Ca2+ flow into the cell. This influx prompts repolarization, closing the channels and preventing further ion entry. The ions stimulate the ryanodine receptor, causing a larger calcium release from the sarcoplasmic reticulum. This activates calmodulin to form a complex that activates myosin light-chain kinase. This phosphorylates the myosin light chain, enabling interaction between actin and myosin. As a result, the smooth muscles contract. However, overactive L-type calcium channels can cause excessive calcium entry into the cells, leading to prolonged vasoconstriction and elevated blood pressure. Calcium channel blockers, such as amlodipine, block the ɑ1 subunit of these channels, inhibiting Ca2+ entry into the cell. This action lowers intracellular calcium levels, relaxing the arterial smooth muscles, reducing peripheral resistance, and ultimately decreasing blood pressure.