What is the pathophysiology of calcium channel blocker (CCB) toxicity?

Updated: Jan 04, 2021
  • Author: B Zane Horowitz, MD, FACMT; Chief Editor: Michael A Miller, MD  more...
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Answer

All existing CCBs function by binding to the L-subtype, voltage-sensitive, slow calcium channels in cell membranes. (Mibefradil, the only T-channel calcium blocker, was withdrawn from the market in 1998 because of multiple drug interactions and risk or death.) [9] The L-type calcium channel blockers decrease the flow of calcium into the cells of the cardiac conduction pathway, which leads to an inhibition of phase 0 in cardiac pacemaker cells and slows the phase 2 plateau in Purkinje cells, cardiac myocytes, and vascular smooth muscle cells. In cardiac muscle and vascular smooth, muscle rapid calcium influx causes myosin and actin binding and contraction. The different classes of CCBs, by inhibiting calcium influx, cause decreased myocardial contractility and peripheral arterial vasodilation.


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