Electrophysiological actions of calcium antagonists in the heart.
Electrophysiological studies have shown that Ca antagonists affect only cardiac structures in which impulse propagation is mediated by the slow channel, i.e., mainly the sinoatrial and atrioventricular nodes. In addition they may depress abnormal slow conduction in diseased fibers. Ca antagonists do not represent a homogeneous group as different compounds seem to have different electrophysiological actions. In man, Ca antagonists normally have no significant effect on sinus node function. However, in patients with sinus node dysfunction, the same drugs may induce dangerous bradycardia or sinoatrial block. These different effects seem to be at least in part due to the different responsiveness of the normal and diseased sinus node to changes in autonomic tone via the baroreceptor reflex. In the A-V node, conduction and refractoriness are prolonged by each Ca antagonist to a different degree. In this regard, D 600 and verapamil have a very strong effect, whereas nifedipine in normal doses does not influence A-V nodal conductivity, and tiapamil and diltiazem have an intermediate position between these extremes. The results may have clinical relevance for antiarrhythmic therapy with Ca antagonists. In addition, they can help to avoid dangerous side effects in patients with disease of the sinus or A-V node.
D001283:Atrioventricular Node / Q000187:drug effects* / Q000502:physiology; D002036:Bundle of His / Q000187:drug effects / Q000502:physiology; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D004594:Electrophysiology; D006329:Heart Conduction System / Q000187:drug effects*; D006801:Humans; D011690:Purkinje Fibers / Q000187:drug effects / Q000502:physiology; D012849:Sinoatrial Node / Q000187:drug effects* / Q000502:physiology
D002121:Calcium Channel Blockers