Antihypertensive Drugs: Action of Calcium Channel Blockers

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.