Homeostasis is the tendency for organisms to regulate automatically and keep their internal environment in a stable state. A stable condition is an optimal functioning condition for an organism, and depends on many variables, such as body temperature and fluid balance, which are stored within predetermined limits. Other variables include extracellular fluid pH, concentrations of sodium, potassium and calcium ions, as well as blood sugar levels, and this needs to be regulated despite environmental changes, diet, or activity levels. Each of these variables is controlled by one or more regulators or homeostatic mechanisms, which together sustain life.
Homeostasis is caused by natural resistance to change under optimal conditions, and balance is maintained by many regulatory mechanisms. All homeostatic control mechanisms have at least three interdependent components for the regulated variable: receptors, control centers, and effector. Receptors are sensing components that monitor and respond to environmental changes, both external and internal. Receptors include thermoreceptors, and mechanoreceptors. Control centers include the respiratory center, and the renin-angiotensin system. An effector is an actionable target, to bring change back to normal. At the cellular level, receptors include nuclear receptors that bring changes in gene expression through up-regulation or down-regulation, and act in negative feedback mechanisms. An example is controlling bile acids in the liver.
Some centers, such as the renin-angiotensin system, control more than one variable. When the receptor senses the stimulus, it reacts by sending the action potential to the control center. The control center sets the maintenance range - acceptable upper and lower limits - for certain variables, such as temperature. The control center responds to the signal by determining the appropriate response and sends the signal to the effector, which can be one or more muscles, organs, or glands. When signals are received and acted upon, negative feedback is given to receptors that stop the need for further signaling.
The concept of internal environmental setting was described by the French physiologist Claude Bernard in 1865, and the word homeostasis was created by Walter Bradford Cannon in 1926. Homeostasis is a biologically almost exclusively term, referring to the concept described by Bernard and Cannon, about the firmness of the internal environment in which the cells of the body live and survive. The term cybernetics is applied to a technological control system such as a thermostat, which functions as a homeostatic mechanism, but is often defined much more broadly than the biological term homeostasis.
Video Homeostasis
Etimologi
The word homeostasis ( ) uses the merge of forms homeo - and -stasis , New Latin from Greek: ?? ???? homoios , "similar" and ?????? stasis , "stand still", generating the idea "remains the same".
Maps Homeostasis
Overview
The metabolic processes of all organisms can only occur in very specific physical and chemical environments. Conditions vary with each organism, and by what chemical processes take place inside the cell or in the interstitial fluid bathing the cell. The most familiar mechanisms of homeostasis in humans and other mammals are regulators that maintain a constant extracellular (or "internal") fluid composition, especially with respect to temperature, pH, osmolality, and sodium, potassium, glucose concentration. , carbon dioxide, and oxygen. However, many other homeostatic mechanisms, which cover many aspects of human physiology, control other entities in the body. Where variable levels are higher or lower than required, they often begin with hyper - and hypo - , each such as hyperthermia and hypothermia and hypertension and hypotension.
If an entity is homeostatically controlled it does not mean that its value is always completely stable in health. The body core temperature, for example, is governed by a homeostatic mechanism with a temperature sensor in, among other things, the hypothalamus of the brain. However, the regulator set point is regularly reset. For example, the core body temperature in humans varies during the day (ie has a circadian rhythm), with the lowest temperatures occurring at night, and the highest in the afternoon. Other normal temperature variations include those associated with the menstrual cycle. The temperature regulating set point is reset during infection to produce a fever. Organisms are able to adjust for varied conditions such as changes in temperature or oxygen levels at altitude, by acclimation process.
Homeostasis does not regulate any activity in the body. For example, signals (either through neurons or hormones) from the sensor to the effector, indispensable, vary widely to convey information about the direction and magnitude of the error detected by the sensor. Similarly the effector response needs to be highly adjusted to reverse the error - in fact it should be very nearly proportional (but in the opposite direction) with errors that threaten the internal environment. For example, arterial blood pressure in mammals is homeostatically controlled, and is measured by stretch receptors in the walls of the aortic arch and carotid sinuses at the beginning of the internal carotid artery. The sensor sends a message through the sensory nerve to the brain's medulla oblongata that indicates whether the blood pressure has dropped or increased, and how much. The medulla oblongata then distributes the message along the motor nerve or euphens belonging to the autonomic nervous system to the various effector organs, whose activity is consequently altered to reverse the error in blood pressure. One effector organ is the heart whose velocity is stimulated to rise (tachycardia) when arterial blood pressure falls, or to slow (bradycardia) when the pressure rises above the set point. Thus the heart rate (which no sensors in the body) is not homeostatically controlled, but is one of the effector's responses to errors in arterial blood pressure. Another example is the level of sweating. It is one of the effector in homeostatic control of body temperature, and therefore varies greatly in the rough proportion to the heat load that threatens to shake the core body temperature, where there are sensors in the hypothalamus of the brain.
Control variables
Core temperature
Mammals regulate their core temperatures using input from thermoreceptors in the hypothalamus, brain, spinal cord, internal organs, and large blood vessels. Regardless of the internal temperature setting, a process called allostasis can come into play that adjusts behavior to adapt to extreme hot or cold challenges (and other challenges). These adjustments can include finding shade and reducing activity, or looking for warmer conditions and increasing activity, or curling up. Thermoregulation behavior takes precedence over physiological thermoregulation because the necessary changes can be affected more quickly and physiologic thermoregulation is limited in its capacity to respond to extreme temperatures.
When the core temperature falls, the blood supply to the skin is reduced by intense vasoconstriction. The blood flow to the limbs (which have large surface area) is also reduced, and returns to the stem through the deep veins located next to the arteries (forming venae comitantes). It acts as a reverse-exchange exchange system that shortens the warmth circuits from arterial blood directly to the veins returning to the stem, causing minimal heat loss from the extremities in cold weather. Subcutaneous intestinal veins are tightened tightly, not only reducing heat loss from this source, but also forcing the venous blood into the counter-current system at the depths of the limbs.
The metabolic rate is increased, initially by non-shivering thermogenesis, followed by tremor of thermogenesis if previous reactions are not sufficient to correct hypothermia.
When the rising core temperature is detected by the thermoreceptors, the sweat glands in the skin are stimulated through the cholinergic sympathetic nerves to secrete sweat to the skin, which, when yawned, cools the skin and blood flows through it. Panting is an alternative effector in many vertebrates, which cools the body also by evaporation of water, but this time from the mucous membranes of the throat and mouth.
Blood glucose
Blood sugar levels are set within fairly narrow limits. In mammals, the main sensor for this is the pancreatic islet beta cells. The beta cells respond to elevated blood sugar levels by secreting insulin into the blood, and simultaneously inhibiting their neighbor's alpha cells from secreting glucagon into the blood. This combination (high blood insulin levels and low glucagon levels) works on effector tissue, which is primarily the liver, fat cells and muscle cells. The liver is inhibited to produce glucose, then pick it up, and turn it into glycogen and triglycerides. Glycogen is stored in the liver, but triglycerides are secreted into the blood as particles of low-density lipoprotein (VLDL) taken by adipose tissue, there to be stored as fat. The fat cells take glucose through a special glucose carrier (GLUT4), whose amount in the cell wall increases as a direct effect of the insulin acting on these cells. The glucose entering the fat cells in this way is converted into triglycerides (via the same metabolic path as the liver uses) and then stored in fat cells along with the VLDL triglycerides made in the liver. Muscle cells also take glucose through the insulin-sensitive GLUT4 glucose channel, and convert it into muscle glycogen.
Decreased blood glucose, causing insulin secretion is stopped, and glucagon is secreted from alpha cells into the blood. This inhibits the uptake of glucose from the blood by the liver, fat cells and muscles. Instead the liver is strongly stimulated to produce glucose from glycogen (via glycogenolysis) and from non-carbohydrate sources (such as lactate and amino acid de-amines) using a process known as gluconeogenesis. So the resulting glucose is thrown into the blood that corrects the detected faults (hypoglycemia). The glycogen stored in the muscle remains in the muscle, and is only broken down, during exercise, into glucose-6-phosphate and from there to pyruvate to be inserted into the citric acid cycle or converted to lactate. Only lactate and waste products from the citric acid cycle are returned to the blood. The liver can only take lactate, and by the process of consuming gluconeogenesis the energy converts it back into glucose.
Iron level
Copper settings
Blood gas level
Changes in oxygen levels, carbon dioxide and plasma pH are sent to the respiratory center, in the brain stem where they are regulated. Partial pressures of oxygen and carbon dioxide in arterial blood are monitored by peripheral chemoreceptors (PNS) in the carotid artery and aortic arch. Changes in partial pressure of carbon dioxide are detected as pH changes in cerebrospinal fluid by the central chemoreceptors (CNS) in the brainstem medulla oblongata. Information from this set of sensors is sent to the respiratory center that activates the effector organ - the diaphragm and other respiratory muscles. Increased levels of carbon dioxide in the blood, or decreased oxygen levels, will result in deeper breathing patterns and increased respiratory rate to restore blood gas to balance.
Too little carbon dioxide, and, to a lesser extent, too much oxygen in the blood can stop breathing temporarily, a condition known as apnea, which freedivers use to extend their time can stay underwater.
Partial pressure of carbon dioxide is more a determinant factor in pH monitoring. However, at high altitudes (above 2500 m), monitoring of partial oxygen pressure is a priority, and hyperventilation keeps oxygen levels steady. With lower levels of carbon dioxide, to keep the pH at 7.4 the kidneys release hydrogen ions into the blood, and secrete bicarbonate into the urine. This is important in acclimatization to high altitude.
Blood oxygen content
The kidneys measure the oxygen content rather than the partial pressure of oxygen in the arterial blood. When the oxygen content in the blood is very low, the oxygen-sensitive cells secrete erythropoietin (EPO) into the blood. The effector tissue is the red bone marrow that produces red blood cells (red blood cells) (erythrocytes). Increased red blood cells cause an increase in hematocrit in the blood, and an increase in hemoglobin which increases oxygen transport capacity. This is the mechanism by which high-altitude inhabitants have higher hematocrit than sea level inhabitants, and also why people with lung insufficiency or right-to-left shunt in the heart (through venous blood through the lungs and directly into circulating systemic) have hematocrit the same height.
Regardless of the partial pressure of oxygen in the blood, the amount of oxygen that can be carried, depends on the content of hemoglobin. Partial pressure of oxygen may be adequate for example in anemia, but hemoglobin levels will not suffice and will then become oxygen content. Given adequate iron supply, vitamin B12 and folic acid, EPO can stimulate RBC production, and hemoglobin and oxygen levels are returned to normal.
Arterial blood pressure
The brain can regulate blood flow through various values ​​of blood pressure with vasoconstriction and arterial vasodilation.
High pressure receptors called baroreceptors in the walls of the aortic arch and carotid sinus (at the beginning of the internal carotid artery) monitor arterial blood pressure. Increased pressure is detected when the artery wall stretches due to an increase in blood volume. This causes the heart muscle cells to release the hormone atrial natriuretic peptide (ANP) into the blood. This action on the kidneys to inhibit the secretion of renin and aldosterone causes sodium release, and accompanies water into the urine, thereby reducing blood volume. This information is then delivered, by afferent nerve fibers, to the solitary nucleus in the medulla oblongata. From here the motor nerves belonging to the autonomic nervous system are stimulated to affect the activity especially the heart and the smallest diameter arteries, called arterioles. Arterioles are the main resistance vessels in the arterial tree, and small changes in diameter cause major changes in the resistance to flow through them. When arterial blood pressure rises, arterioles are stimulated to dilate making it easier for blood to leave the arteries, thus deflating it, and lowering blood pressure, returning to normal. At the same time the heart is stimulated through the cholinergic parasympathetic nerve to pulsate more slowly (called bradycardia), ensuring that blood flow to the arteries is reduced, thereby adding pressure reduction, and original error correction.
Low pressure in the arteries, causing opposite reflexes from arteriolar constriction, and accelerating heart rate (called tachycardia). If the blood pressure drop is very fast or excessive, the medulla oblongata stimulates the adrenal medulla, through the sympathetic "preganglionic" nerves, to secrete epinephrine (adrenaline) into the blood. This hormone increases tachycardia and causes severe vasoconstriction in arterioles to all the vital organs in the body (especially the heart, lungs and brain). These reactions usually correct very low arterial blood pressure (hypotension) very effectively.
Calcium levels
Plasma ionized calcium levels (Ca 2 ) are controlled very closely by a pair of homeostatic mechanisms. The sensors for the first lie in the parathyroid glands, where the head cells sense Ca 2 levels through special calcium receptors in their membranes. The sensor for the second is parafollicular cells in the thyroid gland. Parathyroid head cells secrete parathyroid hormone (PTH) in response to decreased plasma ionized calcium levels; parafollicular cells of the thyroid gland secrete calcitonin in response to elevated plasma ionized calcium levels.
The effector organs of the first homeostatic mechanism are bone, kidney, and, via hormones released into the blood by the kidneys in response to high PTH levels in the blood, duodenum and jejunum. Parathyroid hormone (in high concentrations in the blood) causes bone resorption, releasing calcium into the plasma. This is a very quick action that can correct a threatening hypocalcemia within minutes. High concentrations of PTH lead to excretion of phosphate ions through urine. Because the phosphate combines with calcium ions to form insoluble salts, decreases the level of phosphate in the blood, releasing free calcium ions into the ionized ionized calcium pool. PTH has a second action on the kidneys. It stimulates the preparation and release, by the kidney, from calcitriol into the blood. These steroid hormones work on upper epithelial epithelial cells, increasing their capacity to absorb calcium from the intestinal contents into the blood.
The second homeostatic mechanism, with its sensor in the thyroid gland, releases calcitonin into the blood when the ionised calcium of blood rises. This hormone acts mainly on the bone, causing rapid removal of calcium from the blood and storing it, in its insoluble form, in the bone.
Two mechanisms of homeostasis that work through PTH on the one hand, and calcitonin on the other hand can quickly correct the errors that will occur in plasma ionized calcium levels by removing calcium from the blood and depositing it in bone, or by removing calcium from it.. The framework acts as a very large calcium store (about 1 kg) compared to a plasma calcium store (about 180 mg). Long-term arrangement occurs through absorption or loss of calcium from the gut.
Sodium concentration
The mechanism of homeostasis that controls plasma sodium concentration is somewhat more complex than most other homeostatic mechanisms described on this page.
The sensor is located in a juxtaglomerular kidney device, which senses plasma concentration of the plasma in a surprisingly indirect way. Instead of measuring it directly in blood flowing through the juxtaglomerular cells, these cells respond to sodium concentrations in the renal tubular fluid after which it has undergone a number of modifications in the proximal tubules and the convoluted loop of Henle. These cells also respond to the rate of blood flow through a juxtaglomerular device, which, under normal circumstances, is directly proportional to arterial blood pressure, making this tissue an additional arterial blood pressure sensor.
In response to decreased plasma sodium concentration, or decreased arterial blood pressure, juxtaglomerular cells release renin into the blood. Renin is an enzyme that cuts decapeptide (short chain protein, 10 long amino acids) from a plasma-2-globulin called angiotensinogen. This decapeptide is known as angiotensin I. It has no known biological activity. However, as blood circulates through the lungs, a pulmonary capillary endothelial enzyme called angiotensin-converting enzyme (ACE) intersects two further amino acids from angiotensin I to form an octapeptide known as angiotensin II. Angiotensin II is a hormone that acts on the adrenal cortex, causing release into the blood of the steroid hormone, aldosterone. Angiotensin II also works on smooth muscle in arteriolar walls causing these small diameter vessels to narrow, thus limiting blood flow from arterial trees, causing arterial blood pressure to rise. This is because it reinforces the steps described above (under the heading "Arterial blood pressure"), which maintains arterial blood pressure on changes, especially hypotension.
The angiotensin II-stimulated aldosterone released from the glomerulose zone of the adrenal gland has an effect in particularly the distal convoluted tubule epithelial cells and collects the ductus from the kidney. Here it causes the reabsorption of sodium ions from the renal tubular fluid, in exchange for the potassium ion secreted from the blood plasma to the tubular fluid to escape from the body through the urine. Reabsorption of sodium ions from renal tubular fluid stops further loss of sodium ions from the body, and therefore prevents worsening of hyponatremia. Hyponatremia can only be corrected by the consumption of salt in the diet. However, it is uncertain whether the "hunger for salt" can be triggered by hyponatremia, or by what mechanism this can occur.
When the plasma sodium ion concentration is higher than normal (hypernatremia), the renin release of the juxtaglomerular apparatus is stopped, halting the production of angiotensin II, and consequently the release of aldosterone into the blood. The kidney responds by removing the sodium ions into the urine, thus normalizing the plasma sodium ion concentration. Low levels of angiotensin II in the blood decrease arterial blood pressure as an inevitable concurrent response.
Reabsorption of sodium ions from tubular fluids as a result of high levels of aldosterone in the blood does not, by itself, cause renal tubular water to be returned to the blood from the intricately distal tubules or collecting ducts. This is because sodium is reabsorbed as a substitute for potassium and therefore causes only a small change in the osmotic gradient between the blood and tubular fluid. Furthermore, the distal tubular epithelium is distal and the collecting duct does not penetrate water in the absence of antidiuretic hormone (ADH) in the blood. ADH is part of the fluid balance control. The levels in blood vary with plasma osmolality, as measured in the hypothalamus of the brain. Aldosterone action in the renal tubules prevents sodium loss in extracellular fluid (ECF). Thus there is no change in the osmolality of ECF, and therefore no change in plasma ADH concentration. However, low levels of aldosterone lead to loss of sodium ions from the ECF, potentially leading to changes in extracellular osmolality and therefore the level of ADH in the blood.
Potassium concentration
High concentrations of potassium in the plasma cause the depolarization of the membrane of the glomerulose zone cells in the outer layer of the adrenal cortex. This causes the release of aldosterone into the blood.
Aldosterone acts primarily on distal convoluted tubules and collects ducts from the kidneys, stimulating the excretion of potassium ions into the urine. It does so, however, by activating a basolateral Na /K pump from tubular epithelial cells. This sodium/potassium exchanger pumps three sodium ions out of the cell, into the interstitial fluid and two potassium ions into the cells of the interstitial fluid. This creates an ionic concentration gradient that results in the reabsorption of sodium ions (Na ) from tubular fluid into the blood, and secretes potassium ions (K ) from blood to urine (collecting line lumen).
Liquid balance
The total amount of water in the body must remain balanced. The fluid balance involves keeping the volume of fluid stable, and also keeping electrolyte levels in stable extracellular fluids. The fluid balance is maintained by the osmoregulation process and by behavior. Osmotic pressure is detected by osmoreceptors in the median preoptic nucleus in the hypothalamus. Measurement of plasma osmolality to give an indication of the body's water content, depends on the fact that water loss from the body, (through the inevitable water loss through the skin is not fully water-resistant and therefore always slightly moist, water vapor in the exhaled air, sweating, vomiting, normal stools and especially diarrhea) are all hypotonic, meaning that they are less salty than body fluids (compare, for example, saliva with tears.The latter has almost the same salt content as an extracellular fluid, while the former is hypotonic with plasma.The saliva does not taste salty, while the tears are obviously salty). Almost all normal and abnormal loss of body water therefore causes the extracellular fluid to become hypertonic. In contrast excessive fluid intake melts the extracellular fluid that causes the hypothalamus to register hypotonic hyponatremia conditions.
When the hypothalamus detects a hypertonic extracellular environment, it causes the secretion of the antidiuretic hormone (ADH) called vasopressin acting on the effector organ, which in this case is the kidney. The effect of vasopressin on the renal tubules is to reabsorb the water from the distal tubules that are convoluted and collect the ducts, thus preventing the aggravation of water loss through urine. The hypothalamus simultaneously stimulates the nearby thirst center causing it to be almost unbearable (if hyperbasis is severe enough) to urge for drinking water. Termination of the flow of urine prevents hypovolemia and hypertonicity from getting worse; drinking water fix defects.
Hypo-osmolality produces very low plasma ADH levels. This results in inhibition of the reabsorption of water from the renal tubules, causing a high volume of very dilute urine to be excreted, thus eliminating excess water in the body.
The loss of urine, when the homeostate of the body of water is intact, is the loss of water compensation , corrects any excess water in the body. However, because the kidneys can not produce water, the thirst reflex is the second most important effector mechanism of the body's homeostate, repairing any water deficit in the body.
blood pH
The plasma PH can be altered by respiratory changes at the partial pressure of carbon dioxide; or altered by metabolic changes in carbonic acid to the ratio of bicarbonate ions. The bicarbonate buffer system regulates the ratio of carbonic acid to bicarbonate to 1:20, where the blood pH ratio is 7.4 (as described in the Henderson-Hasselbalch equation). Changes in plasma pH give acid-base imbalance. In acid-base homeostasis there are two mechanisms that can help regulate the pH. Respiratory compensation mechanism of the respiratory center, adjusting the partial pressure of carbon dioxide by changing the rate and depth of breathing, to restore the pH back to normal. The partial pressure of carbon dioxide also determines the concentration of carbonic acid, and the bicarbonate buffer system may also play. Renal compensation may help the bicarbonate buffer system. The sensors for plasma bicarbonate concentration are not known for certain. It is likely that the renal tubular cells from the distal convoluted tubules themselves are sensitive to plasma pH. The metabolism of these cells produces carbon dioxide, which is rapidly converted to hydrogen and bicarbonate through the action of carbonate anhydrase. When the ECF pH falls (becomes more acidic) renal tubular cells secrete hydrogen ions into the tubular fluid to leave the body through the urine. The bicarbonate ion is simultaneously secreted into the blood that lowers the carbonic acid, and consequently increases the plasma pH. The opposite occurs when the plasma pH rises above normal: the bicarbonate ion is excreted into the urine, and the hydrogen ion is released into the plasma.
When hydrogen ions are excreted into the urine, and bicarbonate into the blood, the latter joins the excess hydrogen ion in the plasma that stimulates the kidneys to perform this operation. The reaction produced in the plasma is the formation of carbonic acid which is in equilibrium with the partial pressure of carbon dioxide plasma. This is strictly regulated to ensure that there is no excessive buildup of carbonic acid or bicarbonate. The overall effect is that hydrogen ions are lost in the urine when the plasma pH falls. The simultaneous rise in plasma bicarbonate sweeps up the increase of hydrogen ions (caused by a decrease in plasma pH) and the resulting excess carbonic acid is discharged in the lungs as carbon dioxide. This restores the normal ratio between bicarbonate and partial pressure of carbon dioxide and hence plasma pH. The reverse occurs when high plasma pH stimulates the kidneys to secrete hydrogen ions into the blood and secrete bicarbonate into the urine. The hydrogen ions join the excess of bicarbonate ions in the plasma, again forming excess carbonic acid that can be exhaled, such as carbon dioxide, in the lungs, maintaining the concentration of plasma bicarbonate ions, the partial pressure of carbon dioxide and, therefore, plasma pH, constant.
Cerebrospinal fluid
Cerebrospinal fluid (CSF) allows for the regulation of the intermediate distribution of brain cells, and neuroendocrine factors, which slight changes can cause problems or damage to the nervous system. For example, high glycine concentrations interfere with temperature and blood pressure control, and high CSF pH causes dizziness and syncope.
Neurotransmission
Neurons inhibition in the central nervous system play a homeostatic role in the balance of neuronal activity between excitation and inhibition. The inhibitory neurons use GABA, making compensatory changes in neural networks that prevent escaping excitation rates. The imbalance between excitation and inhibition is seen to be involved in a number of neuropsychiatric disorders.
Neuroendocrine system
The neuroendocrine system is the mechanism by which the hypothalamus maintains homeostasis, regulates metabolism, reproduction, eating and drinking behavior, energy utilization, osmolarity and blood pressure.
Metabolic regulation, performed by interconnecting the hypothalamus to other glands. The three endocrine glands of the hypothalamus-pituitary-gonad axis (the HPG axis) often work together and have important regulatory functions. The other two regulatory endocrine axes are the hypothalamus-pituitary-adrenal axis (HPA axis) and the hypothalamus-pituitary-thyroid axis (HPT axis).
The liver also has many metabolic regulatory functions. An important function is the production and control of bile acids. Too much bile acids can be toxic to cells and their synthesis can be inhibited by FXR activation of nuclear receptors.
Gene rules
At the cellular level, homeostasis is performed by several mechanisms including transcriptional regulation that can alter gene activity in response to change.
Energy balance
The amount of energy taken through the nutrients must match the amount of energy used. To achieve appetite homeostasis energy is regulated by two hormones, grehlin and leptin. Grehlin stimulates hunger and food intake and leptin acts to signal full satiety (fullness).
Clinical interests
Many diseases are the result of homeostatic failure. Almost all homeostatic components can be damaged, either as a result of congenital defects, congenital metabolic error, or acquired disease. Some homeostatic mechanisms have built-in redundancies, which ensure that life is not immediately threatened if components malfunction; but sometimes homeostatic damage can lead to serious illness, which can be fatal if left untreated. A famous example of homeostasis failure is shown in type 1 diabetes mellitus. Here the blood sugar regulation can not function because beta cells from the pancreas island are destroyed and can not produce the required insulin. Blood sugar rises in a condition known as hyperglycemia.
Calcium homeostat calcium plasma can be disturbed by constant, unchanged, over-production of parathyroid hormone by parathyroid adenoma resulting in a characteristic feature of hyperparathyroidism, ie high plasma ionization levels of 2 and bone resorption, which can cause spontaneous fractures. Abnormally high plasma ionized calcium concentrations cause conformational changes in many cell surface proteins (especially ion channels and hormones or neurotransmitter receptors) that cause lethargy, muscle weakness, anorexia, constipation and unstable emotions.
Body water homeostat can be compromised by the inability to secrete ADH in response to even normal daily water loss through exhaled air, impurities, and insensitive sweating. When receiving a zero blood ADH signal, the kidney produces a very large dilute urine volume, leading to dehydration and death if untreated.
As the ages of the organism, the efficiency of their control system becomes lessened. Inefficiencies gradually produce an unstable internal environment that increases the risk of disease, and leads to physical changes associated with aging.
Chronic diseases are controlled by homeostatic compensation, which masks the problem by compensating it in other ways. However, the compensation mechanism is ultimately worn or disturbed by new complication factors (such as the emergence of concurrent acute viral infection), which sends the body shaken through a new cascade of events. The decompensation unmasks the underlying disease, aggravating the symptoms. Common examples include decompensated heart failure, kidney failure, and liver failure.
Biosphere
In the Gaia hypothesis James Lovelock states that the entire mass of living matter on Earth (or any planet with life) functions as a massive super homeostatic superorganism that actively modifies its planetary environment to produce the necessary environmental conditions for its own survival. In this view, the entire planet maintains some homeostats (the primary is temperature homeostasis). Is this kind of system present on Earth open for debate. However, some relatively simple homeostatic mechanisms are generally accepted. For example, it is sometimes claimed that when atmospheric carbon dioxide levels rise, certain plants may be able to grow better and act to remove more carbon dioxide from the atmosphere. However, warming has aggravated the drought, making water a true limiting factor on land. When sunlight is abundant and atmospheric temperature rises, it has been claimed that phytoplankton from sea level, acting as global sunlight, and therefore heat sensors, can develop and produce more dimethyl sulphide (DMS). The DMS molecule acts as a core of cloud condensation, which produces more clouds, and thus increases atmospheric albedo, and this feeds back to lower atmospheric temperature. However, rising ocean temperatures have created a layer of oceans, separating the warm, sun-lit waters from cool, nutrient-rich waters. Thus, nutrients have become a limiting factor, and plankton levels have actually fallen over the last 50 years, rather than increasing. When scientists discover more about Earth, a large number of positive and negative feedback loops are being discovered, that, together, retain metastable conditions, sometimes in a wide range of environmental conditions.
Predictive
Predictive homeostasis is an anticipatory response to expected challenges in the future, such as stimulation of insulin secretion by the intestinal hormone that enters the blood in response to food. This insulin secretion occurs before the blood sugar level rises, lowering the blood sugar level in anticipation of a large influx into the blood of glucose produced from the digestion of carbohydrates in the intestine. Such an anticipatory reaction is an open loop system based on, essentially, on "guesswork," and not self-correcting. Anticipatory responses always require closed loop negative feedback systems to improve 'over-shoots' and 'under-shoots' where anticipatory systems are vulnerable.
More fields
This term has been used in other fields, for example:
Risk
An actuary may refer to homeostasis risks , where (for example) people who have anti-lock brakes do not have a better security record than those who do not have anti-lock brakes, because the former is unconscious compensate for safer vehicles through less secure driving habits. Previously for anti-lock brake innovation, certain maneuvers involve minor skid, evokes fear and avoidance: Now the anti-lock system moves the boundary for that feedback, and the behavior pattern extends to the area that no longer punishes. It has also been argued that the ecological crisis is an example of risk homeostasis in which certain behaviors continue until proven dangerous or dramatic consequences actually occur.
Stress
Sociologists and psychologists may refer to stress homeostasis, the tendency of populations or individuals to remain at a certain level of stress, often resulting in artificial pressure if stress levels are "inadequate".
Jean-Franç§ois Lyotard, a postmodern theorist, has applied this term to the 'centers of social power' which he describes in The Postmodern Condition, as "governed by the principle of homeostasis," eg, hierarchy scientific, which sometimes ignores radical new discoveries over the years for destroying previously accepted rules.
Technology
Familiar homeostatic technological mechanisms include:
- The thermostat operates by switching the heater or AC on and off in response to the output of the temperature sensor.
- The roaming control adjusts the car's throttle in response to speed changes.
- The autopilot operates an aircraft or ship steering control in response to deviations from the pre-defined pads or compass routes.
- Process control systems at chemical plants or refineries maintain fluid levels, pressure, temperature, chemical composition, etc. by controlling heaters, pumps, and valves.
- The steam centrifugal governor, as designed by James Watt in 1788, reduces the throttle valve in response to an increase in engine speed, or opening the valve if speed falls below a predetermined rate.
See also
References
Further reading
- Census, Lucia, ed. (2013). "Chapter 3 Sodium/Potassium Homeostasis, Chapter 5 Calcium Homeostasis, Chapter 6 Manganese homeostasis". Metallomics and Cell . Metal Ion in Life Sciences. 12 . Jumper. doi: 10.1007/978-94-007-5561-1_3. ISBN: 978-94-007-5560-4. ISBN-978-94-007-5561-1 ISSN_ 1559-0836 electronic- ISSN 1868-0402
External links
- Homeostasis
- Walter Bradford Cannon, Homeostasis (1932)
Source of the article : Wikipedia
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