Once<unk>  is ingested, it is absorbed by the gut and metabolized by the liver before it goes into the systemic circulation and reaches the cells of the smooth muscles and cardiac muscle cells. It binds more effectively with L-type calcium channels in smooth muscle cells because of its lower resting membrane potential. The<unk>  diffuses into the membrane and binds to its high affinity binding site on the inactivated L-type calcium channel that's located in between each of the 4 intermembrane components of the α1 subunit. The exact mechanism of action of<unk>  is unknown, but it is believed to have important tyrosine and threonine residues in its binding pocket and its binding interferes with the voltage sensor and gating mechanism of the channel. Thought to have a domain-interface model of binding. In hypertension, the binding of<unk>  causes a decrease in the probability of open L-type calcium channels and reduces the influx of calcium. The reduced levels of calcium prevent smooth muscle contraction within these muscle cells. Prevention of muscle contraction enables smooth muscle dilation. Dilation of the vasculature reduces total peripheral resistance, which decreases the workload on the heart and prevents scarring of the heart or heart failure.<unk>  has additionally been found to act as an antagonist of the mineralocorticoid receptor, or as an antimineralocorticoid.
Nitrendipine
Nadolol
Sodium nitroprusside
Atenolol
Captopril
Isoprenaline
Nisoldipine
Nebivolol