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Regulation of Water Balance in Renal Physiology

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Regulation of Water Balance in Renal Physiology Class: B.Sc. HONOURS ZOOLOGY Paper: Animal Physiology: LSS (Theory Class) Teacher’s name: Meenakshi Rana Date: 2nd May, 2020 Time: 12:30 – 2:30 PM Regulation of water balance in renal physiology As we eat a bite of food, the salivary glands secrete saliva. As the food enters your stomach, gastric juice is secreted. As it enters the small intestine, pancreatic juice is secreted. Each of these fluids contains a great deal of water. How is that water replaced in these organs? What happens to the water now in the intestines? In a day there is an exchange of about 10 liters of water among the body’s organs. The osmoregulation of this exchange involves complex communication between the brain, kidneys, and endocrine system. A homeostatic goal for a cell, a tissue, an organ, and an entire organism is to balance water output with water input. Sources of water gain and loss Total water ouput per day averages 2.5 liters. This must be balanced with water input. Our tissues produce around 300 milliliters of water per day through metabolic processes. The remainder of water output must be balanced by drinking fluids and eating solid foods. The average fluid consumption per day is 1.5 liters, and water gained from solid foods approximates 700 milliliters. Dietary Gain of Water: The Food and Nutrition Board of the Institute of Medicine (IOM) has set the Adequate Intake (AI) for water for adult males at 3.7 liters (15.6 cups) and at 2.7 liters (11 cups) for adult females. It is important to note that the AI for water includes water from all dietary sources; that is, water coming from food as well as beverages. People are not expected to consume 15.6 or 11 cups of pure water per day. The main sources of body water are ingested liquids (about 1600 mL) and moist foods (about 700 mL) absorbed from the gastrointestinal (GI) tract, which total about 2300 mL/day. The other source of water is metabolic water that is produced in the body mainly when electrons are accepted by oxygen during aerobic cellular 1 respiration and to a smaller extent during dehydration synthesis reactions. Metabolic water gain accounts for only 200 mL/day. Daily water gain from these two sources totals about 2500 mL Regulation of Daily Water Input (gain) by Thirst centre Thirst centre: Body water gain is regulated mainly by the volume of water intake, or how much fluid you drink. An area in the hypothalamus known as the thirst center governs the urge to drink. Thirst happens in the following sequence of physiological events: 1. Receptor proteins in the kidney, heart, and hypothalamus detect decreased fluid volume or increased sodium concentration in the blood. 2. Hormonal and neural messages are relayed to the brain’s thirst center in the hypothalamus. 2 3. The hypothalamus sends neural signals to higher sensory areas in the cortex of the brain, stimulating the conscious thought to drink. 4. Fluids are consumed. 5. Receptors in the mouth and stomach detect mechanical movements involved with fluid ingestion. 6. Neural signals are sent to the brain and the thirst mechanism is shut off. Regulation of Daily Water output (loss) There are two types of outputs. The first type is insensible water loss, meaning we are unaware of it. The body loses about 400 milliliters of its daily water output through exhalation. Another 500 milliliters is lost through our skin. The second type of output is sensible water loss, meaning we are aware of it. Urine accounts for about 1,500 milliliters of water output, and feces account for roughly 100 milliliters of water output. Regulating urine output is a primary function of the kidneys, and involves communication with the brain and endocrine system. The kidneys filter about 190 liters of blood and produce (on average) 1.5 liters of urine per day. Urine is mostly water, but it also contains electrolytes and waste products, such as urea. The amount of water filtered from the blood and excreted as urine is dependent on the amount of water in, and the electrolyte composition of, blood. Kidneys have protein sensors that detect blood volume from the pressure, or stretch, in the blood vessels of the kidneys. When blood volume and blood pressure decrease, juxtaglomerular cells in the kidneys secrete the enzyme renin into the blood blood. Renin catalyzes the conversion of angiotensinogen, released by the liver, to angiotensin I. Angiotensin I is in turn hydrolyzed by angiotensin-converting enzyme to form angiotensin II. Angiotensin II targets three different organs (the adrenal glands, the hypothalamus, and the muscle tissue surrounding the arteries) to rapidly restore blood volume and, consequently, pressure. 1. First, angiotensin II travels to the outer perimeter of the adrenal glands and stimulates release of the hormone aldosterone. Aldosterone travels back to the kidneys and stimulates the sodium-potassium pump in the principal cells in the collecting ducts. As a result of the pump’s work, the blood reabsorbs the sodium from the liquid that has already been filtered by the 3 kidneys. Water follows sodium into the blood by osmosis, resulting in less water in the urine and restored fluid balance and composition of blood. 2. Next, angiotensin II travels to the hypothalamus where it stimulates the thirst mechanism and the release of antidiuretic hormone (ADH). Antidiuretic hormone travels back to the kidneys where it increases water reabsorption. ADH released by the posterior lobe of the pituitary plays a role in water reabsorption by the distal convoluted tubule and the collecting duct of the nephron. ADH increases the water reabsorption. In practical terms, if an individual does not drink much water on a certain day, the posterior lobe of the pituitary releases ADH, causing more water to be reabsorbed and less urine to form (antidiuresis). On the other hand, if an individual drinks a large amount of water and does not perspire much, ADH is not released. In that case, more water is exreted and more urine forms (diuresis). Mechanism of action of ADH: When ADH is present in the blood, it binds with its receptor present on the basolateral membrane of a cell in the distal and collecting tubule. This binding activates the synthesis of cAMP (acts as a secondary messenger) within the cells. cAMP increases the insertion of water channels (aquaporin-2) into the membrane. This membrane is impermeable to water in the absence of ADH. After insertion of aquaporin-2, it becomes permeable to water. Water exits from the cell through an open water channel permanently positioned at the basolateral border, and then enters the blood, in this way being reabsorbed. 4 A negative feedback system involving ADH regulates facultative water reabsorption (Figure 26.17). When the osmolarity or osmotic pressure of plasma and interstitial fluid increases—that is, when water concentration decreases—by as little as 1%, osmoreceptors in the hypothalamus detect the change. Their nerve impulses stimulate secretion of more ADH into the blood, and the principal cells become more permeable to water. As facultative water reabsorption increases, plasma osmolarity decreases to normal. A second powerful stimulus for ADH secretion is a decrease in blood volume, as occurs in hemorrhaging or severe dehydration. A deficiency in ADH secretion causes diabetes insipidus in which there is excessive urination (polyuria) and axcessive fluid intake (polydipsia). 3. Lastly, angiotensin II targets smooth muscle tissue surrounding arteries, causing them to contract (narrow) the blood vessels, which assists in elevating blood pressure. 5 Atrial Natriuretic Peptide (ANP) A large increase in blood volume promotes release of ANP from the heart. Although the importance of ANP in normal regulation of tubular function is unclear, it can inhibit reabsorption of Na+ and water in the proximal convoluted tubule and collecting duct. ANP also suppresses the secretion of aldosterone and ADH. These effects increase the excretion of Na+ in urine (natriuresis) and increase urine output (diuresis), which decreases blood volume and blood pressure. 6 .
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