To directly answer your question about hyperkalemia you must think about the inter and extracellular concentration of ions. K (potassium) is the major intracellular ion. Na (sodium) is the major extracellular ion. Membranes of cells are charged lets say -80mV. At this membrane potential, the ionic concentration will be as the body wants it (lots of K in, and Na out)
When we change the concentration of ions in the serum, it will change the membrane potential of ALL cells. Now, all things in the body are transient--there is always some Na entering the cell and some K leaving all to maintain this proper balance.
In the case of hyperkalemia--high concentrations of K in the serum would result in either less K leaving the cell (meaing more positive charges will be in the cell, depolarization) or addional K could enter the cell at high enough K serum concentrations and therefore add more positive charges in the cell and thus depolarize it.
The combining of the neurotransmitter with the muscle membrane receptors causes the membrane to become permeable to sodium ions and depolarization of the membrane. This depolarization triggers an action potential that leads to muscle contraction.
The greater influx of sodium ions results in membrane depolarization. This is because sodium ions carry a positive charge, which leads to a decrease in the membrane potential towards zero or a positive value.
Depolarization in a hair cell is triggered by mechanical stimulation, such as sound waves or movement, while depolarization in a typical neuron is triggered by chemical signals.
The influx of sodium ions causes depolarization of the cell membrane, making the interior less negative. This depolarization can trigger the opening of voltage-gated ion channels, leading to the propagation of an action potential. Sodium-potassium pumps work to restore the original ion concentrations, repolarizing the cell.
Depolarization is the process where the membrane potential becomes less negative, moving towards zero or even becoming positive. This occurs when sodium ions rush into the cell. Repolarization is the return of the membrane potential back to its resting state, following depolarization, usually through the efflux of potassium ions from the cell.
The nerve impulse causes the release of acetylcholine from the motor end plate. This causes the depolarization of the membrane of the adjacent muscle cell.
The combining of the neurotransmitter with the muscle membrane receptors causes the membrane to become permeable to sodium ions and depolarization of the membrane. This depolarization triggers an action potential that leads to muscle contraction.
The greater influx of sodium ions results in membrane depolarization. This is because sodium ions carry a positive charge, which leads to a decrease in the membrane potential towards zero or a positive value.
A QRS wave is caused by the depolarization of the ventricles of the heart, which leads to the contraction of the ventricles and the pumping of blood out of the heart. The QRS complex represents the electrical activity associated with this depolarization.
depolarization of the presynaptic membrane due to an arriving action potential
The depolarization phase of an action potential in neurons is primarily caused by the rapid influx of sodium ions through voltage-gated sodium channels. This influx of sodium ions results in the membrane potential becoming more positive, leading to depolarization of the neuron.
Local depolarization is caused by the opening of voltage-gated sodium channels in response to the binding of neurotransmitters or other stimuli. This influx of sodium ions results in membrane depolarization, reaching the threshold potential needed to generate an action potential.
Binding of acetylcholine to nicotinic acetylcholine receptors opens ion channels that allow both sodium and potassium ions to permeate the membrane. This causes depolarization of the membrane potential, leading to an excitatory response in the cell.
In excitable cells such as neurons and muscle cells, the movement of ions across the cell membrane causes polarization and depolarization. Specifically, during polarization, the cell interior becomes more negative due to the influx of potassium ions. In contrast, depolarization involves the influx of sodium ions, leading to a reversal of the membrane potential towards a more positive charge.
Depolarization in a hair cell is triggered by mechanical stimulation, such as sound waves or movement, while depolarization in a typical neuron is triggered by chemical signals.
When acetylcholine (ACh) receptors open, sodium ions (Na+) primarily flow into the postsynaptic membrane. This influx of positively charged sodium ions leads to depolarization, making the inside of the cell more positive. If the depolarization reaches a certain threshold, it can trigger an action potential in the postsynaptic neuron.
The nerve impulse causes the release of acetylcholine from the motor end plate. This causes the depolarization of the membrane of the adjacent muscle cell. Depolarization triggers the release of calcium ions from the sarcoplasmic reticulum inside the muscle cell. In the presence of ATP, the high calcium level causes the myosin heads to bend, dragging actin filaments towards the middle of the unit of contraction.