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Function Kidney Nephron Animation

 function kidney nephronin the human body normally

1. Urine Production And Blood Filtration
(1) Blood with waste enters the kidney through the renal artery. The artery divides into smaller and smaller blood vessels, called arterioles, eventually ending in the tiny capillaries of the glomerulus in each of the Nephrons.

(2) The Blood in kidney get into glomerulus through Affarent Arteriole. In glomerulus, blood travel through twist and turn capilaries. The capillary walls here are quite thin, and the blood pressure within the capillaries is high. The result is that water, along with any substances that may be dissolved in it typically salts, glucose or sugar, amino acids, and the waste products urea and uric acid are pushed out through the thin capillary walls, where they are collected in Bowman's capsule.

kidney function blood test
Larger particles in the blood, such as red blood cells and protein molecules, are too bulky to pass through the capillary walls and they remain in the bloodstream. The blood, which is now filtered, leaves the glomerulus through Everent Arteriole, which branches into the meshlike network of blood vessels around the renal tubule. The blood then exits the kidney through the renal vein. Approximately 180 liters (about 50 gallons) of blood moves through the two kidneys every day.

(3) Urine production begins with the substances that the blood leaves behind during its passage through the kidney the water, salts, and other substances collected from the glomerulus in Bowman’s capsule. This liquid, called glomerular filtrate, moves from Bowman’s capsule through Proximal Convulated Tubule. As the filtrate flows through the renal tubule, the network of blood vessels surrounding the tubule reabsorbs much of the water, salt, and virtually all of the nutrients, especially glucose and amino acids, that were removed in the glomerulus. This important process, called tubular reabsorption, enables the body to selectively keep the substances it needs while ridding itself of wastes. Eventually, about 99 percent of the water, salt, and other nutrients is reabsorbed. This process happens in Henle’s Loop.

(4) At the same time that the kidney reabsorbs valuable nutrients from the glomerular filtrate, it carries out an opposing task, called tubular secretion. In this process, unwanted substances from the capillaries surrounding the nephron are added to the glomerular filtrate. These substances include various charged particles called ions, including ammonium, hydrogen, and potassium ions. The secretion of potassium by the distal tubule is one of the most important events in the dikney as its control is fundamental to the maintance of overall potassium balance.

(5) Together, glomerular filtration, tubular reabsorption, and tubular secretion produce urine, which flows into collecting ducts, which guide it into the microtubules of the pyramids. The urine is then stored in the renal cavity and eventually drained into the ureters, which are long, narrow tubes leading to the bladder. From the roughly 180 liters (about 50 gallons) of blood that the kidneys filter each day, about 1.5 liters (1.3 qt) of urine are produced.

2. Body’s Water Volume Regulator
Other kidney’s essential function is to regulate the amount of water contained in the blood. This process is influenced by antidiuretic hormone (ADH), also called vasopressin, which is produced in the hypothalamus (a part of the brain that regulates many internal function) and stored in the nearby pituitary gland. Receptors in the brain monitor the blood’s water concentration. When the amount of salt and other substance in the blood becomes to high, the pituitary gland release ADH into the bloodstream.

The blood contained ADH from the brain flow and get into the kidney. In the presence of ADH the renal tubules and colecting ducts become freely permeable to solute and water. It cause more water reabsorbed into the bloodstream. On the other hand in the absence of ADH the collecting ducts are impermeable to solute and water; thus, the fluid in the lumen, from which some solute has been remove, remains less concentrated than plasma; the urine is dilute.

3. Blood Pressure Regulator
Regulating blood pressure is linked to the kidneys' ability to excrete enough sodium chloride (salt) to maintain normal sodium balance, extracellular fluid volume and blood volume. Kidney disease is the most common cause of secondary hypertension (high blood pressure). Even minor disruptions in kidney function play a role in most (if not all) cases of high blood pressure and increased injury to the kidneys. This injury can eventually cause malignant hypertension, stroke or even death.

In normal people, when there's a higher intake of sodium chloride (salt), the body adjusts. It excretes more sodium without raising arterial pressure. However, many outside influences can reduce the kidneys' ability to excrete sodium. If the kidneys are less able to excrete salt with normal or higher salt intake, chronic increases in extracellular fluid volume and blood volume result. This leads to high blood pressure. When there is an increase in hormones and neurotransmitters that cause blood vessels to narrow, even small increases in blood volume are compounded. (This is due to the smaller area of blood vessel through which the blood is forced to flow.) Although the increases in arterial pressure lead the kidneys to excrete more sodium (which restores the sodium balance), higher pressure in the arteries may persist. This shows the important link between kidney disease and high blood pressure.

The hormone aldosterone, produced by the adrenal glands, interacts with the kidneys to regulate the blood’s sodium and potassium content. High amounts of aldosterone cause the nephrons to reabsorb more sodium ions, more water, and fewer potassium ions; low levels of aldosterone have the reverse effect. The kidney’s responses to aldosterone help keep the blood’s salt levels within the narrow range that is best for crucial physiological activities.

Aldosterone also helps regulate blood pressure. When blood pressure starts to fall, the kidney releases an enzyme (a specialized protein) called renin, which converts a blood protein into the hormone angiotensin. This hormone causes blood vessels to constrict, resulting in a rise in blood pressure. Angiotensin then induces the adrenal glands to release aldosterone, which promotes sodium and water to be reabsorbed, further increasing blood volume and blood pressure.

4. Body’s Acid Base Balance
The kidney also adjusts the body’s acid base balance to prevent such blood disorders as acidosis and alkalosis, both of which impair the functioning of the central nerveous system. If the blood is too acidic, meaning that there is an excess of hydrogen ions, the kidney moves these ions to the urine through the process of tubular secretion.

5. Production of Hormones
1) Erythropoietin
Several hormones are produced in the kidney. One of these, erythropoietin, influences the production of red blood cells in the bone marrow. When the kidney detects that the number of red blood cells in the body is declining, it secretes erythropoietin. This hormone travels in the bloodstream to the bone marrow, stimulating the production and release of more red cells.

Erythropoietin is a glycoprotein. It acts on the bone marrow to increase the production of red blood cells. Stimuli such as bleeding or moving to high altitudes (where oxygen is scarcer) trigger the release of EPO. People with failing kidneys can be kept alive by dialysis. But dialysis only cleanses the blood of wastes. Without a source of EPO, these patients suffer from anemia. Now, thanks to recombinant DNA technology, recombinant human EPO is available to treat these patients.

Because EPO increases the hematocrit, it enables more oxygen to flow to the skeletal muscles. Some cyclists (and distance runners) have used recombinant EPO to enhance their performance. Although recombinant EPO has exactly the same sequence of amino acids as the natural hormone, the sugars attached by the cells used in the pharmaceutical industry differ from those attached by the cells of the human kidney. This difference can be detected by a test of the athlete's urine.

Prolonged exposure to reduced oxygen levels (e.g., living at high altitude) leads to increased synthesis of EPO. In mice, and perhaps in humans, this effect is mediated by the skin. Mouse skin cells can detect low levels of oxygen ("hypoxia") and if this persists, blood flow to the kidneys diminishes leading to increased synthesis of EPO by them.

Recently it has been found that EPO is also synthesized in the brain when oxygen becomes scarce there (e.g., following a stroke), and helps protect neurons from damage. Perhaps recombinant human EPO will turn out to be useful for stroke victims as well.
2) Calcitriol
Calcitriol is 1,25[OH]2 Vitamin D3, the active form of vitamin D. It is derived from calciferol (vitamin D3) which is synthesized in skin exposed to the ultraviolet rays of the sun
precursors ("vitamin D") ingested in the diet. Calciferol in the blood is converted into the active vitamin in two steps:
i. calciferol is converted in the liver into 25[OH] vitamin D3
ii. this is carried to the kidneys (bound to a serum globulin) where it is converted into calcitriol. This final step is promoted by the parathyroid hormone (PTH).

Calcitriol acts on the cells of the intestine to promote the absorption of calcium from food. Calcitriol acts also in the bone to mobilize calcium from the bone to the blood Calcitriol enters cells and, if they contain receptors for it (intestine cells do), it binds to them. The calcitriol receptors are zinc-finger transcription factors. Insufficient calcitriol prevents normal deposition of calcium in bone.

In childhood, this produces the deformed bones characteristic of rickets. In adults, it produces weakened bones causing osteomalacia.The most common causes are inadequate amounts of the vitamin in the diet or insufficient exposure to the sun.However, some rare inherited cases turn out to be caused by inheriting two mutant genes for the kidney enzyme that converts 25[OH] vitamin D3 into calcitriol.Other cases of inherited rickets (also very rare) are caused by inheriting two defective genes for the calcitriol receptor. Mutations that change the amino acids in one or another of the zinc fingers interfere with binding to the DNA of the response element.
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