Electrophysiological effects of α₂-adrenergic stimulation in canine cardiac Purkinje fibers

The effects of α₂-adrenergic stimulation on action potentials were measured in isolated canine Purkinje fibers. Action potential durations at 50 and 90% of repolarization (APD₅₀ and APD₉₀) were significantly prolonged by 0.25 μM l-norepinephrine + 0.5 μM dl-propranolol (NE + P) from baseline values of 165 ± 7 and 249 ± 9 (SE) ms (n = 7) to 174 ± 7 and 265 ± 9 ms, respectively (P < 0.05 for both). Selective α₂-blockade with 0.01 μM yohimbine (YO) reduced this prolongation by NE + P in APD₅₀ and APD₉₀ to 169 ± 7 and 256 ± 8 ms, respectively (P < 0.05 compared with NE + P). Additional selective α₁-blockade with 0.01 μM prazosin (PZ) completely blocked the effects of NE + P, returning APD₅₀ and APD₉₀ to 163 ± 7 and 250 ± 9 ms (not different from baseline). After incubation of isolated Purkinje fibers with pertussis toxin (1 μg/ml), which reduced the availability of a 41-kDa membrane protein for ADP ribosylation by 70 ± 7% (n = 4, P < 0.05), YO failed to reverse the prolongation in action potential durations brought on by NE + P, but the effects of PZ were intact. The effects of α₂-stimulation on β-adrenergic-induced delayed afterdepolarizations (DADs) were studied by burst pacing of Purkinje fibers in Tyrode solution containing 7.5 mM Ca²⁺. The DADs induced in the presence of NE + PZ (B- + α₂-stimulation) were significantly smaller in amplitude and required a shorter pacing cycle length to reach threshold than those induced in the presence of NE + PZ + YO (unopposed β-adrenergic stimulation). Furthermore sustained triggered activity, seen in five of eight preparations under β-stimulation, could no longer be elicited in the presence of β- + α₂-stimulation. These results suggest that the postjunctional α₂-adrenergic receptors in canine Purkinje fibers are coupled to a pertussis toxin-sensitive G protein and that stimulation of these receptors leads to action potential prolongation and suppression of DADs induced by β-adrenergic stimulation.