Cardiac Muscle Study Questions Bank

Myocardial contractility refers to the strength and force of contraction of the heart muscle. Calcium ions play a crucial role in regulating myocardial contractility. During the cardiac cycle, calcium ions are released from the sarcoplasmic reticulum into the cytoplasm of the cardiac muscle cells. This increase in intracellular calcium concentration leads to the activation of the contractile proteins, resulting in the contraction of the heart muscle. Therefore, the intracellular concentration of Ca2+ is best correlated with myocardial contractility.

During the plateau phase of the ventricular action potential, the membrane potential is most dependent on calcium permeability. This is because during this phase, the influx of calcium ions through L-type calcium channels is responsible for maintaining the prolonged depolarization and preventing repolarization. The calcium influx balances the outward potassium current, resulting in a stable membrane potential. Therefore, the membrane potential during the plateau phase is highly influenced by calcium permeability.

During the plateau phase of the ventricular action potential, the conductance to Ca2+ is the highest. This is because during this phase, the L-type calcium channels are open, allowing an influx of calcium ions into the cell. This influx of calcium ions plays a crucial role in maintaining the depolarized state of the cell and prolonging the action potential. The high conductance to Ca2+ during the plateau phase is important for various physiological processes, including muscle contraction and regulation of cardiac output.

Connexin is an important component of the gap junction. Gap junctions are specialized intercellular channels that allow direct communication and exchange of small molecules between adjacent cells. Connexin proteins form these channels by assembling into hexameric structures called connexons. These connexons on one cell align with connexons on the adjacent cell, creating a channel for the passage of ions, small molecules, and electrical signals. Therefore, connexin plays a crucial role in facilitating intercellular communication and coordination.

During the process of excitation-contraction coupling in cardiac muscle, calcium is released from the sarcoplasmic reticulum primarily by an increase in intracellular calcium concentration. This increase in calcium concentration triggers the release of calcium from the sarcoplasmic reticulum, which then binds to troponin and initiates the contraction of the cardiac muscle. Inositol triphosphate (IP3) and protein kinase A do not directly contribute to the release of calcium from the sarcoplasmic reticulum in this process. An increase in intracellular sodium concentration is not involved in the release of calcium from the sarcoplasmic reticulum.

In the sinoatrial (SA) node, phase 4 depolarization (pacemaker potential) is attributable to an increase in Na+ conductance. This means that during this phase, there is an increase in the flow of sodium ions into the cell, which leads to depolarization and the initiation of the action potential. This increase in Na+ conductance is responsible for the spontaneous and rhythmic firing of the SA node, which serves as the natural pacemaker of the heart.

The depolarization phase of the action potential in a ventricular muscle cell is produced by the inward Na+ current. During this phase, the voltage-gated Na+ channels open, allowing an influx of Na+ ions into the cell. This influx of positive ions depolarizes the cell membrane, bringing it closer to the threshold for an action potential. The inward Na+ current is responsible for the rapid upstroke of the action potential in ventricular muscle cells.

The delay between the atrial and ventricular contractions is mainly caused by the slow action potential conduction velocity of AV nodal cells. The AV node acts as a gatekeeper, allowing a delay in the electrical signal to ensure that the atria contract and empty their blood into the ventricles before the ventricles contract. This delay allows for efficient filling of the ventricles and prevents backflow of blood into the atria. The slow conduction velocity of the AV nodal cells is necessary for this coordination between the atria and ventricles.

current is carried into the cell primarily by relatively slow Ca++ currents instead of by fast Na+ currents.
There are, in fact, no fast Na+ channels and currents operating in SA nodal cells.

Cardiac E-C Coupling is the process by which electrical signals are transmitted to the contractile apparatus of the heart, resulting in contraction. In this process, extracellular calcium is indeed required to initiate contraction, as it enters the cell through L-type calcium channels (DHP receptors) and triggers the release of calcium from the sarcoplasmic reticulum via the ryanodine receptor (RyR). Calcium then binds to troponin, allowing for cross-bridge cycling and muscle contraction. ATP is required for the removal of calcium from the cytoplasm, which is accomplished by the primary active Na+/K+ pumps creating a concentration gradient that the secondary active Na+/Ca2+ exchanger utilizes to remove calcium from the cytoplasm. Therefore, the statement "All DHP receptors are mechanically coupled to RyR" is not true.

The correct temporal sequence for excitation-contraction coupling in cardiac muscle is as follows: depolarization of the muscle sarcolemma, Ca2+ influx through DHP receptors, Ca2+ activated Ca2+ release from RyR in the SR, cross-bridge cycling, Ca2+ removal from SR by SERCA, PMCA, and Na/Ca exchanger. This sequence accurately represents the order of events that occur during excitation-contraction coupling in cardiac muscle, starting with depolarization and ending with the removal of Ca2+ from the sarcoplasmic reticulum.

Phase 4 is the spontaneous depolarization (pacemaker potential) that triggers the action potential once the membrane potential reaches threshold between -40 and -30 mV).

The plateau phase of the action potential from a ventricular muscle is the result of approximately equal inward and outward currents. This means that the flow of positively charged ions into the cell is balanced by the flow of positively charged ions out of the cell. This balanced current allows for an extended period of depolarization, which helps to sustain muscle contraction and ensure effective pumping of blood by the heart.

The statement that the ions responsible for the depolarizing upstroke is Na+ and Ca2+ in both types of action potentials is not true. In neuronal action potentials, the depolarizing upstroke is primarily due to the influx of Na+ ions, while in cardiac action potentials, it is primarily due to the influx of Ca2+ ions.

Inhibition of Na/K ATPase would result in increased intracellular Ca2+ concentration. Na/K ATPase is responsible for maintaining the concentration gradients of Na+ and K+ across the cell membrane. By actively pumping Na+ out of the cell and K+ into the cell, Na/K ATPase helps to maintain a low intracellular Na+ concentration and a high intracellular K+ concentration. Inhibition of Na/K ATPase would disrupt this balance, leading to an increase in intracellular Na+ concentration. This increase in intracellular Na+ concentration would then impair the function of the Na/Ca exchanger, causing an increase in intracellular Ca2+ concentration.

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The upstroke of the action potential in Purkinje fibers is the result of an inward Na+ current. This is because during the upstroke, there is a rapid influx of Na+ ions into the cell, which depolarizes the membrane and leads to the initiation of the action potential.

The DHP receptor does not require the hydrolysis of ATP to function properly. The DHP receptor, also known as the dihydropyridine receptor, is a voltage-gated calcium channel found in muscle cells. It plays a crucial role in the excitation-contraction coupling of skeletal and cardiac muscles. Unlike the other options listed, which are all involved in active transport processes and require ATP hydrolysis for their function, the DHP receptor functions as a passive calcium channel and does not directly utilize ATP.

During the resting phase of the ventricular action potential, the membrane is closest to the K+ equilibrium potential. This is because at rest, the membrane potential is close to the K+ equilibrium potential, which is typically around -90 mV. During the other phases of the action potential (depolarization, plateau, repolarization), the membrane potential deviates from the K+ equilibrium potential due to the movement of other ions such as Na+ and Ca2+.

L-type calcium channels in cardiac ventricular muscle cells are responsible for allowing calcium entry that triggers sarcoplasmic reticulum calcium release, and they open in response to depolarization of the membrane. They are also found in the T-tubule membrane and are open during the plateau phase of the action potential. However, they do not contribute to the pacemaker potential, which is generated by the funny current (If) channels.

During the ventricular action potential, the phase that coincides with diastole is "At rest". Diastole is the phase of the cardiac cycle when the heart muscle relaxes and fills with blood. At rest, the ventricles are not contracting and are in a relaxed state, allowing them to fill with blood. This phase occurs between contractions and is essential for adequate blood flow and cardiac function.

The channel opened by ACh when it binds to receptors on the end plates of skeletal muscle fibers is equally permeable to potassium and sodium. The increase in sodium permeability allows sodium to flow into the cell and produces the end-plate potential.
-The plateau phase of ventricular muscle action potentials and the upstroke of smooth muscle action potentials are produced by an increase in calcium conductance.
- An increase in potassium conductance is responsible for the downstroke of the action potential.
- The refractory period is caused by an increase in potassium conductance and a decrease in the number of sodium channels available to produce an action potential (i.e., sodium channel inactivation).

-Upstroke phase of AP in smooth muscle is caused by calcium.

-Plateau phase of cardiac muscle is caused by Calcium.

-Upstroke phase of skeletol muscle is caused by Sodium.