calcium and muscle SDL Flashcards
is sodium higher intracellularly or extracellularly in the resting membrane potential
high extracellularly, low intracellularly
is potassium higher intercellularly or extracellular in the resting membrane potential
high intracellularly, low extracellularly
is calcium higher intracellu.arly or extracellularly in the resting membrane potential
high extracellularly, low intracellularly
in the resting membrane potential, what ions are concentrated inside the cell vs outside the cell
potassium inside the cell
calcium and sodium outside the cell
outline the role calcium plays in nerve conduction
Resting stage: - 90mV negative potential
Depolarisation stage: membrane is permeable to Na ions, which flow inwards
Repolarisation stage: Na channels close and the K channels become more permeable allowing K to flow outwards and re-establish the normal negative resting membrane potential.]
A deficit of calcium (hypocalcaemia) causes the sodium voltage gated channels to be activated with very little increase in membrane potential. Calcium binds to the exterior of the sodium channel and alters the electrical state of the channel protein itself, thereby altering the voltage required to open the sodium gate.
The nerve fibre can become very excitable and fire repetitively without stimulation. The ionized calcium concentration only need fall below 50% of normal before spontaneous discharge may occur in some peripheral nerve, i.e. muscle “tetany”. Tetanic contraction of the respiratory muscles may prove fatal.
what role does calcium play in the neuromuscular synapse/junction
An action potential opens voltage-gated Ca-channels at the nerve terminal at the neuromuscular synapse. This allows the calcium concentration inside the terminal to increase by ~100 fold. This increases the rate of fusion of acetylcholine (ACh) vesicles with the terminal membrane by ~10,000 fold. Exocytosis of the ACh into the synaptic terminal occurs, the ACh then binds to ACh-gated ion channels in the post-synaptic muscle membrane, and an influx of sodium ions generates an end plate potential. This, in turn, initiates an action potential along the muscle membrane.
what are the mechanisms involved in the contraction of skeletal muscle
Excitation-contraction coupling – the action potential is transmitted from the muscle surface through transverse tubules. Calcium ions are released in the immediate vicinity of the myofibrils from the sarcoplasmic reticulum. The calcium binds with troponin C, which initiates the contraction process. The inhibitory effect of the troponin-tropomyosin complex on the actin filaments is inhibited by calcium; leading to muscle contraction via the “walk along” or “ratchet” theory.
what are the mechanisms involved in the contraction of smooth muscle
Similar to skeletal muscle, the initiation of smooth muscle contraction is an increase in intracellular calcium ions. This increase may be a result of nerve or hormonal stimulation of the smooth muscle fibre, stretch of the fibre, or changes in the chemical environment of the fibre.
In smooth muscle, the regulatory protein troponin is replaced with calmodulin:
1. Calmodulin interacts with four calcium ions.
2. The calmodulin-calcium complex joins, and activates, myosin kinase.
3. Myosin kinase phosphorylates the regulatory chain on each myosin head.
4. The phosphorylated myosin head can now bind the actin filament and enter the attachment-release-reattachment cycle to cause smooth muscle contraction.
what are the mechanisms involved in the contraction of cardiac muscle
Similar to skeletal muscle, excitation-contraction coupling allows an action potential to cause myocardial contraction. The action potential spreads over the cardiac muscle membrane and into the interior via the transverse (T) tubules. The T tubule action potential then acts on the longitudinal sarcoplasmic tubules to cause release of calcium from the sarcoplasmic reticulum into the muscle sarcoplasm. Calcium ions diffuse into the myofibrils and catalyze the chemical reactions that allow actin and myosin filaments to interact and result in a muscle contraction.
The T tubules of cardiac muscle have 25 times the volume of skeletal muscle T tubules, and also store and contribute to the calcium ion influx at the time of the action potential to increase cardiac muscle contractility.
How do structural differences between skeletal and cardiac muscle affect the responsiveness of the muscle to extracellular fluid (ECF) calcium concentrations (i.e., blood calcium levels)?
Skeletal muscle – the T tubules have closed ends. The calcium ions that initiate a skeletal muscle contraction are released from the sarcoplasmic reticulum from within the skeletal muscle fibre. Therefore, skeletal muscle is not affected as much by the ECF calcium concentration.
Cardiac muscle – the ends of the T tubules open directly to the outside of the cardiac muscle fibres, allowing the same extracellular fluid in the cardiac muscle interstitium to enter the T tubules. Therefore, the availability of calcium ions to cause cardiac muscle contraction is dependent on the ECF calcium
explain how calcium is involved in the increased cardiac contractility induced by catecholamines
noreprinephrine causes the cardiac muscle fibre membrane to become more pereable to calcium. this increases contractile strength because of their role in exciting the contractile process of the myofibrils
Based on the physiological role of calcium in muscle contraction, explain what clinical signs in respect to skeletal muscle you would expect in a bitch with eclampsia (puerperal tetany).
In a bitch with puerperal tetany (eclampsia) the ionized calcium level in the blood drops. The deficit in calcium causes permeability changes to voltage-gated Ca2+ and Na+ channels. It increases influx of Na+ into the cell causing changes to the cells resting membrane potential. The cell becomes more easily ‘excitable’, it requires a stimulus of lesser magnitude to become depolarized. The nerve fibre becomes more excitable; small stimuli, which would have been ineffective in the past, produce depolarization and generation of impulses which lead to repeated stimulation of skeletal muscles and contraction. In more severely affected cases it will lead to tetanic muscle contraction.
The clinical signs related to the effect on muscle are: mild tremors, twitching, muscle spasms, stiffness and ataxia. In severe cases severe tremors, tetany and seizures can be seen.
