Possible Interaction: Calcium Channel Blockers and Potassium

“In direct comparison with ACEIs or ARBs (11 trials), CCBs increased GFR [MD 11.07 mL/min (95% CI 6.04-16.09)] and reduced potassium levels but were not more effective in reducing BP.”

“ECGs from 145 patients receiving a combined potassium and sodium channel blocking agent for conversion of atrial fibrillation (AF), underwent semiautomatic analysis in a digitalized high-precision analysis program.”

“Antiarrhythmic drugs class IA (quinidine, disopyramide), … (sotalol, amiodarone), class IV calcium channel blockers ) used at the … time with potassium depleters diuretics or beta-blocking agents result in the inhibition of repolarization and the increased duration … activation potential with the risk of developing arrhythmia of the torsade de pointes types.”

“The calcium channel antagonists , nifedipine, verapamil and diltiazem (0.01-10 microM), inhibited responses to high potassium , and the initial phase of shortening and lengthening responses to noradrenaline.”

“ Potassium chloride-induced contractions were completely inhibited by the calcium channel blockers diltiazem and nifedipine or by excluding Ca2+ from the medium.”

“Minor lowering of plasma potassium levels during a CA regimen was exceptional and a rise of plasma uric acid values never reported; the latter may even decrease under certain circumstances.”

“Contractions which were triggered by action potentials or depolarizing extracellular potassium concentrations were highly sensitive to calcium channel blockers.”

“In pial arteries the calcium antagonists nifedipine and nimodipine caused an almost complete relaxation of contractions induced by potassium at drug concentrations relaxing prostaglandin F2α-contracted vessels to only about 60%.”

“A combined use of potassium and calcium antagonists may reduce the frequency-dependence of the pure class III antiarrhythmic drug.”

“The types of calcium channels present at the synaptic terminal were determined by the inhibitory action of calcium channel blockers on potassium‐induced [3H]GABA release in the same cell preparation.”