title: Peculiarities of AV nodal conduction and the role of slow Na current.
abstract: Atrioventricular (AV) conduction was studied in isolated, perfused rabbit hearts. Total AV interval was subdivided into the intraatrial, intranodal and His-Purkinje conduction times. Concentrations of Ca, K and Na in the control perfusate were 2.4, 4.5 and 144.8 mM, respectively. Generalized ischemia or hypoxia almost selectively depressed intranodal conduction, engendering a second degree block. Low Ca (0.8 mM) slightly prolonged the intranodal conduction time, whereas high Ca (4.8-7.2 mM) caused a greater prolongation of this interval, often causing intranodal block. High Ca-induced depression of intranodal conduction was antagonized by high K (7.5 mM). Verapamil (0.5-1.0 mg/L) produced a second degree intranodal block. Subsequent elevation of Na concentration to 172 mM (but not high Ca) restored a 1:1 conduction. Tetrodotoxin (2-10 mg/L) did not affect, whereas low Na (108.6 mM) severely depressed intranodal conduction. These results suggest that (1) AV nodal conduction is most vulnerable to reduced oxygen supply, (2) an optimal Ca concentration for AV nodal conduction exists, (3) high K counteracts high Ca-induced depression of AV nodal conduction, and (4) slow Na current may play a major role in generating AV nodal action potentials. Voltage clamp experiments on the AV node substantiated some of these observations.
mesh_terms: D000200:Action Potentials; D000818:Animals; D001283:Atrioventricular Node / Q000187:drug effects / Q000502:physiology*; D002118:Calcium / Q000037:antagonists & inhibitors / Q000494:pharmacology; D006329:Heart Conduction System / Q000502:physiology*; D000860:Hypoxia / Q000503:physiopathology; D066298:In Vitro Techniques; D007511:Ischemia / Q000503:physiopathology; D011817:Rabbits; D012964:Sodium / Q000502:physiology*; D014700:Verapamil / Q000494:pharmacology
chemical_list: D012964:Sodium; D014700:Verapamil; D002118:Calcium