The excitability of epinephrine-induced slow responses in rabbit atrial trabeculae.
Slow responses were induced in isolated rabbit left atrial trabeculae in a medium containing 20 mM K+ and 1.8 microM epinephrine. Under these conditions, the Na+-dependent upstroke of the cardiac action potential is absent but it is possible to obtain tetrodotoxin-resistant Ca2+-action potentials (slow responses). Conventional electrophysiological techniques were employed for stimulating the preparation and measuring transmembrane potentials. Under these experimental conditions, slow responses exhibit frequency-dependent excitability changes. The excitability of epinephrine-induced slow responses increases with increasing stimulation frequency. This increase is manifested by a decrease in the latency of the slow response and also by a decrease in the stimuli requirements. In this respect, slow responses induced by epinephrine are similar to barium-induced slow responses. These observations provide further support for the hypothesis that the Ca2+-inflow during slow response electrogenesis promotes an increase in slow response excitability. These results are discussed in relation to the propagation of the slow response through the atrioventricular node under physiological conditions.
D000818:Animals; D001283:Atrioventricular Node / Q000187:drug effects*; D001464:Barium / Q000494:pharmacology*; D004837:Epinephrine / Q000494:pharmacology*; D006321:Heart / Q000187:drug effects*; D006325:Heart Atria / Q000187:drug effects; D006329:Heart Conduction System / Q000187:drug effects*; D066298:In Vitro Techniques; D011188:Potassium / Q000494:pharmacology; D011817:Rabbits; D013268:Stimulation, Chemical
D001464:Barium; D011188:Potassium; D004837:Epinephrine