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One of two lower chambers of the heart.
In higher vertebrates, the left ventricle receives arterial blood from the left atrium and pumps it into the aorta, and the right ventricle receives venous blood from the right atrium and pumps it into the pulmonary artery.
Systole, or contraction of the heart is initiated by the electrical cells of the sinoatrial node, which is the heart's natural pacemaker.
These cells are activated spontaneously by depolarization of their membranes beyond a certain threshold for excitation.
At this point, voltage-gated calcium channels on the cell membrane open and allow calcium ions to pass through, into the sarcoplasm, or interior, of the muscle cell.
Some calcium ions bind to receptors on the sarcoplasmic reticulum causing an influx of calcium ions into the sarcoplasm.
The calcium ions bind to the protein troponin, causing a conformational change and breaking the interaction between the troponin-tropomyosin protein complex and filamentous actin (F-actin).
This allows the myosin heads to bind to their respective binding sites on F-actin, and contraction results as the myosin heads draw the actin filaments along, are bound by ATP, causing them to release the actin, and return to their original position, breaking down the ATP into ADP and a phosphate group.
The action potential spreads via the passage of sodium ions through the gap junctions that connect the sarcoplasm of adjacent myocardial cells.
The neurotransmitter norepinephrine (noradrenaline) is released by the terminal boutons of depolarized sympathetic fibers, at the sinoatrial and atrioventricular nodes.
Norepinephrine diffuses across the synaptic cleft and binds to the extracellular binding pocket of β1-adrenoreceptors – G protein-coupled receptors (GPCRs), also called seven-transmembrane receptors because their polypeptide chain crosses the membrane seven times – converting them to their active state.
The receptor changes its conformation and activates the G-protein on the intracellular side of the membrane.
The activated G-protein promotes the production of 3',5'-cyclic adenosine monophosphate (cAMP) through the activation of the enzyme adenylate cyclase.
cAMP is a second messenger which in turn activates protein kinase A.
Protein kinase A phosphorylates the calcium ion channels in the sarcolemma (the membrane of a muscle fiber cell), so that calcium ion influx is increased when they are activated by the appropriate transmembrane voltage.
This will cause more of the calcium receptors in the sarcoplasmic reticulum to be activated, creating a larger flow of calcium ions into the sarcoplasm (an example of positive feedback).
More troponin will be bound and more myosin binding sites cleared [of tropomyosin] so that more myosin heads can be recruited for the contraction and a greater force and speed of contraction results.
[Phosphodiesterase catalyses the hydrolysis of cAMP to AMP, so that it is no longer able to activate protein kinase A.]
Noradrenaline also affects the atrioventricular node, reducing the delay before continuing conduction of the action potential via the bundle of HIS.
Cardiac Diastole is the period of time when the heart relaxes after contraction in preparation for refilling with circulating blood.
Ventricular diastole is when the ventricles are relaxing, while atrial diastole is when the atria are relaxing.
Together they are known as complete cardiac diastole.
During ventricular diastole, the pressure in the (left and right) ventricles drops from the peak that it reaches in systole.
When the pressure in the left ventricle drops to below the pressure in the left atrium, the mitral valve opens, and the left ventricle fills with blood that was accumulating in the left atrium.
Likewise, when the pressure in the right ventricle drops below that in the right atrium, the tricuspid valve opens and the right ventricle fills with blood that was in the right atrium.
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