Block 3 Cardiac And Smooth Muscle Function

Tetanic twitches are typically seen in skeletal muscle but not in cardiac muscle. Skeletal muscle has the ability to undergo sustained contractions, known as tetanic twitches, where the muscle fibers are stimulated at a high frequency and do not have enough time to relax fully between contractions. This allows for smooth and continuous movements. In contrast, cardiac muscle undergoes rhythmic contractions to pump blood and does not exhibit tetanic twitches.

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In the given scenario, the increase in pressure causes Ca2+ entry into smooth muscle cells through stretch-sensitive Ca2+ channels. Once Ca2+ enters the cells, it binds to calmodulin. Calmodulin is a protein that plays a crucial role in regulating smooth muscle contraction. When Ca2+ binds to calmodulin, it activates the calmodulin-dependent protein kinase, which then initiates the contraction of smooth muscle cells. Therefore, in this case, the contraction is initiated by Ca2+ binding to calmodulin.

Both skeletal muscle and smooth muscle share the characteristic of elevation of intracellular [Ca++] for excitation-contraction coupling. This means that an increase in the concentration of calcium ions inside the muscle cells is necessary for the contraction of both types of muscles. Calcium ions play a crucial role in triggering the interaction between the thick and thin filaments, leading to muscle contraction.

During the contraction and relaxation of cardiac muscle, calcium is released from the sarcoplasmic reticulum to initiate muscle contraction. After contraction, calcium needs to be removed from the cytoplasm to allow for muscle relaxation. This removal of calcium is achieved through the process of primary active transport, where energy from ATP is used to pump calcium ions back into the sarcoplasmic reticulum against their concentration gradient. This process ensures that the calcium levels in the cytoplasm are kept low, allowing for proper muscle relaxation.

In skeletal muscle, the action potential and contraction have similar durations, allowing for the sustained contraction known as tetanic contraction. However, in cardiac muscle, the action potential and contraction have different durations. The action potential in cardiac muscle is longer than the contraction, which prevents tetanic contractions from occurring. This is important for the proper functioning of the heart, as it allows for relaxation and refilling of the chambers between contractions.

Diltiazem is a class IV antiarrhythmic drug that blocks voltage-gated Ca+ channels. The AV node of the heart relies on these Ca+ channels for the initiation and conduction of action potentials. By blocking these channels, diltiazem directly inhibits the initiation or action potential in the AV node, leading to a decrease in conduction velocity and contractility. This ultimately results in a decrease in heart rate and can be used to treat certain arrhythmias.

During the contraction and relaxation of smooth muscle, the crossbridge cycling is ended by the dephosphorylation of myosin molecules. This dephosphorylation process allows the myosin heads to detach from actin filaments, leading to muscle relaxation. Phosphorylation of myosin molecules is actually necessary for the initiation of crossbridge cycling, not its termination. The movement of tropomyosin over myosin binding sites and restoration of normal resting membrane potential are not directly involved in ending crossbridge cycling. Storage of all calcium ions within the sarcoplasmic reticulum is important for muscle relaxation, but it does not directly end crossbridge cycling.

The upstroke phase of action potentials refers to the rapid depolarization of the cell membrane. In cardiac AV nodal tissue, the flow of calcium into the cell is necessary for the upstroke phase of action potentials. This influx of calcium ions triggers the opening of voltage-gated sodium channels, leading to the depolarization of the cell membrane and the initiation of the action potential. In contrast, in cardiac ventricular muscle, skeletal muscle fibers, nerve cell bodies, and presynaptic nerve terminals, the upstroke phase of action potentials is primarily mediated by the flow of sodium ions into the cell.

The acetylcholine receptors on smooth muscle are G-protein linked. G-protein linked receptors are a type of cell surface receptor that activate intracellular signaling pathways through the activation of G-proteins. These receptors are involved in a variety of physiological processes, including muscle contraction. In the case of acetylcholine receptors on smooth muscle, the binding of acetylcholine to the receptor activates a G-protein, which then initiates a signaling cascade leading to muscle contraction.

Smooth muscle is unique in that the regulation of excitation-contraction coupling occurs on the thick filament. In skeletal and cardiac muscles, regulation primarily occurs on the thin filament. This means that in smooth muscle, the interaction between actin and myosin is regulated by factors associated with the thick filament, such as myosin light chain phosphorylation. In contrast, in skeletal and cardiac muscles, regulation is primarily mediated by the binding of calcium to tropomyosin on the thin filament. Additionally, smooth muscle does not require extracellular calcium for contraction, unlike skeletal and cardiac muscles.

An increase in preload leads to an increase in the amount of blood filling the heart before contraction. This increased filling stretches the muscle fibers, allowing for a stronger contraction and therefore an increase in shortening velocity. Afterload, on the other hand, refers to the resistance the heart must overcome to eject blood. An increase in afterload would make it more difficult for the heart to contract and shorten, resulting in a decrease in shortening velocity. Therefore, the relationship between preload, afterload, and muscle fiber shortening velocity is that an increase in preload leads to an increase in shortening velocity, while an increase in afterload causes a decrease in shortening velocity.