Histamines
Increased capillary permeability
Active potential, often referred to as action potential, is a rapid change in the membrane potential of a neuron or muscle cell that occurs when the membrane becomes permeable to ions, primarily sodium (Na+) and potassium (K+). During the depolarization phase of the action potential, the membrane's permeability to Na+ increases, allowing these ions to flow into the cell, which causes a rapid rise in membrane potential. This is followed by repolarization, where the permeability to K+ increases, allowing K+ to exit the cell, restoring the membrane potential to its resting state. Thus, active potential is closely linked to the dynamic changes in ion permeability of the membrane.
Histamine released from mast cells primarily causes vasodilation and increased vascular permeability. This leads to the widening of blood vessels, resulting in increased blood flow to the affected area, which contributes to redness and swelling. Additionally, the increased permeability allows proteins and fluids to leak into surrounding tissues, facilitating the inflammatory response. These effects are crucial in the body's response to allergens and infections.
Release of histamine causes dilation of blood vessels, increased vascular permeability, and smooth muscle contraction. This can result in symptoms such as itching, redness, swelling, and bronchoconstriction depending on the location of release and the receptors it activates.
Yes, hypercalcemia causes nervous system depression - the opposite of (see below) According to the Human Anatomy and Physiology Textbook by Marieb, hypocalcemia causes neuron excitation and if severe enough, leads to tetany and then paralysis. this is because both serum calcium and intracellular calcium are increased. The reason hypocalcemia causes neuron excitation (contrary to the above logic) is because a decrease in extracellular calcium concentration increases the neuron membrane's permeability to sodium and allows sodium to easily depolarize the neuron's membrane and cause an action potential. Additionally The membrane threshold becomes refractory to depolarization thus many of the symptoms are related to the loss of cell membrane excitability. How extracellular calcium controls sodium membrane permeability is another question.
vasodilation causes increased pressure within the blood vessel which causes gaps within endothelium to form-this allows for the increased permeability.
Increased capillary permeability
Active potential, often referred to as action potential, is a rapid change in the membrane potential of a neuron or muscle cell that occurs when the membrane becomes permeable to ions, primarily sodium (Na+) and potassium (K+). During the depolarization phase of the action potential, the membrane's permeability to Na+ increases, allowing these ions to flow into the cell, which causes a rapid rise in membrane potential. This is followed by repolarization, where the permeability to K+ increases, allowing K+ to exit the cell, restoring the membrane potential to its resting state. Thus, active potential is closely linked to the dynamic changes in ion permeability of the membrane.
Histamine released from mast cells primarily causes vasodilation and increased vascular permeability. This leads to the widening of blood vessels, resulting in increased blood flow to the affected area, which contributes to redness and swelling. Additionally, the increased permeability allows proteins and fluids to leak into surrounding tissues, facilitating the inflammatory response. These effects are crucial in the body's response to allergens and infections.
Release of histamine causes dilation of blood vessels, increased vascular permeability, and smooth muscle contraction. This can result in symptoms such as itching, redness, swelling, and bronchoconstriction depending on the location of release and the receptors it activates.
Electric energy cause a membrane to move by turning into mechanical energy. The movement of the membrane causes the air pressure to besequentially increased and rarefied. This "train" of increased and rearefied air pressure propagates into the room, and if it strikes our ear drums we perceive it as sound.
When a signal molecule activates a transport protein on the cell membrane, it undergoes a conformational change that opens a channel or alters its affinity for the molecule it transports. This allows specific substances to move across the membrane, facilitating cellular communication and maintaining homeostasis.
Red blood cells can lyse in thiourea due to the compound's ability to disrupt the integrity of the cell membrane. Thiourea can alter the membrane's fluidity and permeability, leading to an imbalance in osmotic pressure. This causes water to rush into the cells, resulting in swelling and eventual rupture. Additionally, thiourea can denature proteins, further compromising the structural integrity of the membrane.
Yes, hypercalcemia causes nervous system depression - the opposite of (see below) According to the Human Anatomy and Physiology Textbook by Marieb, hypocalcemia causes neuron excitation and if severe enough, leads to tetany and then paralysis. this is because both serum calcium and intracellular calcium are increased. The reason hypocalcemia causes neuron excitation (contrary to the above logic) is because a decrease in extracellular calcium concentration increases the neuron membrane's permeability to sodium and allows sodium to easily depolarize the neuron's membrane and cause an action potential. Additionally The membrane threshold becomes refractory to depolarization thus many of the symptoms are related to the loss of cell membrane excitability. How extracellular calcium controls sodium membrane permeability is another question.
gravity and soil permeability (spaces in between sand particles)
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.
Increasing extracellular potassium (K+) reduces the concentration gradient between the inside and outside of the cell, leading to a decrease in the driving force for potassium to exit the cell. As a result, the membrane potential becomes less negative (depolarizes) because the resting membrane potential is influenced by the relative permeability of the membrane to potassium ions. This outcome aligns with the prediction that an increase in extracellular potassium would diminish the negativity of the membrane potential, confirming the importance of K+ concentration gradients in maintaining resting membrane potential.