Calcium channel blockers act on slow ca++ channels known as voltage gated calcium channels. These channels basically allow entry of calcium into cells. Calcium is used up for process of contraction. With calcium channel blockers this entry into cells is prevented. As a result of this muscle contraction is slowed down.
Specifically speaking, ca++ channel blockers decrease phase 0 and phase 4 of action potential in cardiac muscle. It has also its effect at SA node and AV node. In these fibers conduction velocity is decreased and refractory period is increased. Refractory period refers to the phase of action potential during which another action potential can not be generated.
Calcium channel blockers are used for converting atrio-ventricular nodal entry back to normal sinus rhythm.
On blood vessels ca++ channel blocker decreases contraction resulting in increase in their diameter. This leads to decrease of peripheral arterial resistance.
Combined effect of slowed contraction of heart and decrease of peripheral resistance leads decrease output of heart. Blood pressure also drops as a result of it since it is determined by cardiac output and peripheral resistance.
In contrast to ca++ channel blockers, beta blockers affect on sympathetic activity. This is achieved by the action of beta blockers on reduced production of cAMP, which leads to reduced sodium and calcium currents and thereby suppression of abnormal pacemaker activity if there is any. Decreased rate of firing of sympathetic system also decreases heart rate.
Calcium channel blockers may cause baroreceptor response that is when ca++ channel blockers are used alone, when they decrease blood pressure, reflexively there is activity of baroreceptors, which leads to increased rate of firing of heart. Beta blockers may be combined with calcium channel blockers to decrease effects of baroreceptor responses that may arise as a result of use of calcium channel blockers.