What Is Passive Transport?

Passive transport is a mode of transport in which substances follow a concentration gradient without consuming cellular metabolic energy (ATP). The driving force for transportation comes from the potential gradient energy or potential difference of the concentration gradient of substances inside and outside the plasma membrane. Passive transportation is divided into simple diffusion and facilitation diffusion. ^[1]

Facilitated diffusion, also known as assisted diffusion, is a means of transporting substances along a concentration gradient with the help of transport proteins on the membrane. Hydrophilic nutrients such as glucose, amino acids, nucleotides, and charged ions such as Na ⁺ , K ⁺ , Ca ²⁺ can be transported across the membrane through easy diffusion. Transport proteins that mediate facilitation diffusion include carrier proteins and channel proteins. According to this, facilitation diffusion is divided into carrier protein-mediated facilitation diffusion and channel protein-mediated facilitation diffusion. Proteins that mediate active transport are also called carrier proteins.

Carrier protein-mediated facilitation diffusion

Transport is achieved through reversible conformational changes in the carrier protein. Carrier protein is a transmembrane protein on the membrane that is related to the transport of substances. It is highly selective for the substance being transported. When the specific binding site on one end surface of the carrier protein binds to a specific solute molecule, it causes the spatial conformational change of the carrier protein to transport The solute molecule is transported from one side of the binding to the other side of the membrane; the affinity of the allosteric carrier protein to the transported substance changes at the same time, so the transported solute molecule is separated from the carrier protein and released, and the carrier protein is restored to The original conformation. Carrier proteins are repeatedly used through repeated conformational changes.

The rate of facilitation diffusion depends on the difference between the two solute molecules in the membrane. As the concentration difference increases, the speed of transport increases, but when the site where the solute molecule binds to the carrier protein saturates, the transport rate reaches saturation and does not increase. The activity of carrier proteins can be regulated, with hormones playing a major regulatory role.

Most mammalian cell membranes contain a glucose transporter (GLUT) that assists the diffusion of glucose from the blood into the cell. It can transport glucose to human cells in a way that facilitates diffusion. Glucose transporters, the number of which is equivalent to 5% of the total membrane protein, the maximum transfer rate is about 180 glucose molecules per second. The glucose transporter family includes GLUT1-GLUT14, all of which are involved in glucose transport. GLUT1 is distributed on the plasma membrane of a variety of cells and has a high affinity for glucose, making it easy for glucose to be absorbed into human cells. GLUT2 is mainly distributed in hepatocytes, islet -cells (rodents), and intestinal epithelial cells with absorption function in the small intestine and kidney. The combination of GLUT2 with glucose has high blistering degree and low affinity. GLUT3 is distributed in neuron cells in the brain and has a high affinity for glucosamine and transportation capacity. Even when the blood glucose level is slightly low, it can quickly transport glucose from extracellular fluid to ensure the energy supply of neurons. GLUT4 is distributed on the membranes of muscle cells and fat cells, and insulin can regulate the amount of GLUT4. Under normal circumstances, GLUT4 of target cells is stored in cells in the form of vesicles. When blood glucose increases after a meal, it stimulates islet cells to secrete insulin, and insulin stimulates target cells, so that intracellular vesicles containing GLUT4 quickly move to the cell surface. GLUT4 is inserted into the plasma membrane to increase glucose uptake and ensure stable blood glucose. On the contrary, when the body is starved, the blood glucose concentration decreases. Under the action of glucagon, liver glycogen is degraded to produce a large amount of glucose. The concentration of glucose in the cell is higher than that in the cell. Glucose binds to the binding site inside the carrier protein cell. On the other hand, the bamboo shoots were transported outside the cell. Diabetic patients are often accompanied by insufficient GLUT4 quantity or decreased function. When blood glucose rises, glucose cannot enter human target cells smoothly, leading to continuous increase in blood glucose, which is one of the reasons for insulin resistance. ^[1]

Channel protein-mediated facilitation diffusion

Transport is accomplished by means of a channel protein that traverses the lipid bilayer. Channel protein centers are hydrophilic pores, and different types of channel proteins can transport small molecules such as ions and water, respectively. Channel proteins that mainly transport ions are also called ion channels, which have a high affinity and selectivity for ions. Ion channels have high transport rates, transporting millions of ions per second, and carrier proteins carrying less than a thousand molecules per second. Some ion channel protein stars are closed and open when they undergo a conformational change when they are stimulated by a specific signal. The opening time does not exceed a few milliseconds, and then they close.

According to the gate ion channel opening signal, it is divided into 3 types. The first type is a voltage gate channel. The opening and closing of the channel are controlled by changes in membrane potential, such as Na ⁺ channels, K ⁺ channels, and so on. The second type is the ligand gate channel. The opening and closing of the channel are regulated by chemicals. The more in-depth research is the acetylcholine receptor channel. The third type is stress-activated channels. Channel proteins sense conformational stress and change their conformation, opening channels. For example, the auditory hair on the top of the auditory hair cells of the inner ear has this channel. Sound wave stimulation is converted into mechanical vibration in the cochlea, which can cause the hearing hair to tilt and affect the stress-activated K ⁺ channel on the hair. K ⁺ flows into the inner ear hair cells. Depolarize hair cells and produce auditory signals.

The momentary switching of the gate ion channel is conducive to the sequential execution of various functional activities of the cell. During the entire reaction process of skeletal muscle contraction caused by nerve impulses, at least 4 kinds of gate ion channels are sequentially activated, and they are sequentially opened and closed.

When the impulse reaches the nerve endings, the nerve cell membrane depolarizes, and the membrane potential decreases, causing the voltage gate Ca ²⁺ channel on the nerve ending membrane to open, and the high concentration of Ca ²⁺ outside the membrane quickly enters the nerve endings, stimulating the secretory neurotransmission Quality-acetylcholine.

The released acetylcholine binds to a specific part of the ligand gate channel on the muscle cell membrane, and the gate opens instantly, and a large amount of Na ⁺ enters the cell, causing the muscle cell membrane potential to change and the membrane to be partially depolarized.

The local depolarization of the muscle cell membrane makes the voltage gate Na ⁺ channels on the membrane open, more Na ⁺ enters the muscle cells, and the depolarization extends to the entire muscle cell membrane.

The depolarization of the muscle cell membrane causes the Ca ²⁺ channels on the sarcoplasmic network in the muscle cells to open, and the cytoplasm flows from the sarcoplasmic network. The Ca ²⁺ concentration in the muscle cells rises sharply, causing myofibrils to contract. ^[1]