Cardiac Muscle Contractions
CARDIAC MUSCLE CONTRACTIONS
- Cardiac muscle contra ction initiated by Ca2+
Mechanism of contraction:
- Increase in cytoplasmic/sarcoplasmic Ca2+—-> Causes contraction.
Steps:
On action potential development,
↓
Ca2+ influxes within cardiac cell.
- Via L-type Ca2+ channels in sarcolemma.
↓
Influx triggers Ca2+ release from sarcoplasmic reticulum to sarcoplasm.
- Via ryanodine receptors.
↓
Increases intracellular Ca2+
↓
Causing cardiac muscle contraction.
Mechanism during relaxation:
- Decreased cytoplasmic/sarcoplasmic Ca2+ –> Cardiac muslce relaxation.
- Ca2+ conc. reduced by 2 mechanisms,
- Pumping back Ca2+ into SR.
- Done by Sarcoplasmic reticulum calcium pump/SR-Ca2+ATPase/SRCA.
- Also by, Ca2+-3Na+ antiport in sarcolemma.
PHOSPHOLAMBAN:
- Regulatory protein in cardiac muscles.
- Attaches & inactivates SRCA in its dephosphorylated state.
- Normally SRCA transports Ca2+ into SR lumen.
- Causing muscle relaxation.
Phosphorylation of phospholamban:
- Activated by β-adrenergic stimulation.
- Enzyme involved – Protein kinase ‘A’.
Effects of phospholamban phosphorylation:
- Causes cardiac muscle relaxation
- By relieving inhibitory effect of phospholamban on SRCA.
- Resulting in increased Ca2+ uptake into sarcoplasmic reticulum from sarcoplasm.
- This decreases sarcoplasmic Ca2+concentration
- Hence accelerates relaxation.
- Reduces cardiac cycle duration.
- Positive chronotropic effect:
- Increases heart rate.
Effects of phospholamban dephosphorylation:
- Produces two effects –
- Direct:
- Positive chronotropic effect:
- Acceleration of relaxation causing increased heart rate.
Indirect:
- Positive inotropic effect:
- Increased contraction.
- Resultant of increased Ca2+ sequestration in SR.
- Hence, phospholamban “Critical Repressor of Myocardial Contractility”
In response to β-adrenergic/sympathetic stimulation:
- Phospholamban “brake” is released.
- Rapid increase in both contraction & relaxation.
- As in “Fight or Flight” response.
Note:
- Type of calcium channels in skeletal, smooth & cardiac muscles – L-type channels.
Exam Question
CARDIAC MUSCLE CONTRACTIONS
- Cardiac muscle contraction are initiated by Ca2+.
- Increased cytoplasmic/sarcoplasmic Ca2+ cause contraction.
- AP generation causes Ca2+ influx within cardiac cell via L-type of Ca2+ channels in sarcolemma.
- Ca2+ influx triggers Ca2+ release from sarcoplasmic reticulum to sarcoplasm via ryanodine receptors.
- Phospholamban is the regulatory protein present in cardiac muscles.
- Normally sarcoplasmic reticulum calcium pump/SR Ca2+- ATPase/SRCA, transports Ca2+ into SR lumen causing muscle relaxation.
- Phosphorylation of phospholamban is activated by β-adrenergic stimulation with help of protein kinase ‘A’.
- On phospholamban phosphorylation, its inhibitory effect on SRCA is relieved.
- This causes increased Ca2+ uptake into sarcoplasmic reticulum from sarcoplasm of cardiac muscles.
- Also produces positive chronotropic effect – Increased heart rate.
- Phospholamban is called “Critical Repressor of Myocardial Contractility”.
- Because of positive inotropic effect.
- Type of calcium channels in skeletal, smooth & cardiac muscles – L-type channels.
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