Modulation of slow response excitability by calcium in rabbit atrial trabeculae.
Slow responses were induced in rabbit isolated left atrial trabeculae in a modified Tyrode solution containing 15 mM-KCl and 1 mM-BaCl2. Conventional electrophysiological techniques were employed for stimulating and recording membrane potentials. Under these conditions, the excitability of the slow response depends on the past excitatory history of the preparation. As the stimulation frequency increases (range: 0.08-1 Hz) for a conditioning period of stimulation, the excitability of the slow response increases. This can be demonstrated by a decrease in stimulus requirement necessary to maintain slow response excitation following the conditioning period of stimulation. It is shown that when extracellular Ca2+ concentration is reduced to 0.5 mM, that phenomenon of frequency-dependent slow response excitability disappears but slow responses can still be elicited. Also, the addition of D-600 to 2.7 mM-Ca2+ solutions depresses both the slow response and its frequency-dependent excitability. The absence of frequency-dependent slow response excitability is not related to the depression of the slow response upstroke caused by low-Ca2+ solutions. Increasing intracellular Ca2+ concentration by exposing the preparation to low-Na+ solutions or to ouabain did not revert the observed effects in low-Ca2+ solutions. The addition of substances (5 mM-caffeine or 0.35 microM-adrenaline) that potentiate the influx of Ca2+ in low-Ca2+ solutions was found to be effective in restoring the dependence of slow response excitability on the frequency of stimulation. The increase in extracellular Ca2+ above 4 mM depressed the excitation of the slow response. Above 5.4 mM-Ca2+, the excitation of the slow response was completely inhibited while the preparation displayed continuous oscillations in transmembrane potential. The presence of a subthreshold response (subliminal response) that precedes and triggers slow response excitation is accompanied by tension development. Since the subliminal response is responsible for the changes in slow response excitability it is proposed that the Ca2+ inflow during slow response electrogenesis modulates the excitability of the slow response. Two possible physiological implications for this finding are discussed.
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002110:Caffeine / Q000494:pharmacology; D002118:Calcium / Q000494:pharmacology*; D004837:Epinephrine / Q000494:pharmacology; D005711:Gallopamil / Q000494:pharmacology; D006321:Heart / Q000502:physiology*; D066298:In Vitro Techniques; D007537:Isometric Contraction; D011817:Rabbits; D012964:Sodium / Q000494:pharmacology; D013324:Strontium / Q000494:pharmacology; D013997:Time Factors
D005711:Gallopamil; D002110:Caffeine; D012964:Sodium; D002118:Calcium; D004837:Epinephrine; D013324:Strontium