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Synaptic delay in the heart: an ionophoretic study.

I Hill-Smith, R D Purves

    The Journal of Physiology
    |June 1, 1978
    PubMed
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    Neurotransmitters like acetylcholine and noradrenaline affect heart muscle cell beating rates. Long latencies suggest cell membrane processes, not drug diffusion, mediate these neurotransmitter responses.

    Area of Science:

    • Cardiology
    • Neuropharmacology
    • Cell Physiology

    Background:

    • Understanding neurotransmitter effects on cardiac cells is crucial for cardiovascular research.
    • Neonatal rat ventricular cells offer a model for studying cellular responses to neurotransmitters.
    • Autonomic nerve stimulation in adult rat atria provides a comparative model.

    Purpose of the Study:

    • To investigate the effects of neurotransmitters on cultured neonatal rat ventricular muscle cells.
    • To characterize the latency and duration of cellular responses to specific neurotransmitters.
    • To explore the mechanisms underlying the observed response times, differentiating between diffusion and cellular processes.

    Main Methods:

    • Ionophoresis of neurotransmitters (acetylcholine, carbachol, noradrenaline, adrenaline, isoprenaline) onto cultured rat ventricular cells.

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  • Measurement of spontaneous beating rates and cellular membrane potential changes.
  • Comparison of cultured cell responses with chronotropic responses in intact adult rat atria.

    • Main Results:

    • Acetylcholine and carbachol caused hyperpolarization and decreased beating rate with ~250 msec latency.
    • Noradrenaline, adrenaline, and isoprenaline increased beating rate with 3-6 sec latency, with prolonged effects.
    • Response time courses in cultured cells mirrored those in intact atria.
    • Diffusion limitations were ruled out as the cause of long latencies, suggesting membrane-associated processes.
    • Intracellular cyclic AMP application did not mimic catecholamine effects.

    Conclusions:

    • The long latencies of neurotransmitter effects on heart muscle cells are likely due to membrane-bound physical or chemical processes.
    • Drug diffusion to receptors is not the rate-limiting step for these responses.
    • Further research is needed to elucidate the precise intracellular mechanisms involved in neurotransmitter signaling in cardiac cells.