Activation of a transient outward current (Ito) in elephant seal atrial fibres is related to triggered release of Ca2+ from the sarcoplasmic reticulum, generating phasic tension.
Membrane currents and development of tension in atrial trabeculae from elephant seal hearts were studied using a single sucrose-gap voltage-clamp technique. A transient outward current (Ito) was observed with kinetics, voltage and beat dependence, similar to those of tension. Ito had a bell-shaped voltage dependence similar to that of tension and the slow inward current (Isi). Ito, unlike Isi, showed beat dependence quite similar to developed tension. Increases in Cao, frequency of stimulation, and addition of adrenaline enhanced Ito and developed tension. Ito was suppressed by addition of Mn2+, tetracaine, or by depolarizing pre-pulses (to -40 mV for 250 ms). Caffeine at low concentrations (1 mM) blocked beat dependence of Ito. At higher concentrations (greater than 5 mM) caffeine suppressed the activation of Ito, phasic tension, and the second component of the birefringence signal (related to Ca2+-releasing activity of the sarcoplasmic reticulum (s.r.]. Similar to Isi phasic tension and Ito, the voltage dependence of the second component of the birefringence signal was bell-shaped. Our studies suggest that activation of Ito is related to triggered release of Ca2+ from the s.r. which generates the phasic tension. An excitation-contraction coupling scheme is presented which incorporates these findings and suggests that Ito may be responsible for shorter action potentials found in atrial fibres.
Maylie et al. (Sat,) conducted a other in Elephant seal atrial fibres. Voltage-clamp technique and pharmacological agents (adrenaline, Mn2+, tetracaine, caffeine) was evaluated on Membrane currents (Ito) and development of tension. Activation of a transient outward current (Ito) in elephant seal atrial fibres is related to triggered release of Ca2+ from the sarcoplasmic reticulum, generating phasic tension.