Key Points
- Investigate the membrane currents responsible for the initiation of contraction and relaxation in bullfrog ventricular trabeculae.
- Assessed membrane potentials, currents, and contractile tension in bullfrog ventricular trabeculae using the double glycerol-gap voltage-clamp technique.
- Evaluated tension kinetics and membrane currents under graded sodium depletion and in the constant presence of tetrodotoxin (10⁻⁷ g/ml).
- Fast sodium current contributed less than 6% of maximum tension, indicating the slow inward current system is primarily responsible for initiating twitch contractions.
- Depleting sodium by 50% markedly augmented active slow inward current and contractile tension while lowering threshold voltages, demonstrating calcium-sodium antagonism.
- Complete sodium depletion caused sustained tonic contracture and steady outward current, whereas sodium reintroduction produced steady inward current and accelerated relaxation by decreasing the time constant.
Structured PICO
PPopulationBullfrog ventricular trabeculae
IInterventionVoltage clamp using double glycerol-gap technique, tetrodotoxin exposure (10-7g/ml), and Na-depletion
CComparatorBaseline conditions / normal external Na concentration
OOutcomeMembrane potentials, currents, and contractile responsessurrogate
In bullfrog ventricular trabeculae, the slow inward current initiates phasic contraction, while Na-Ca exchange mechanisms mediate tonic contraction and relaxation.