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Chapter 19.docx

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Chapter 19 - The Urinary System: Fluid and Electrolyte Balance Factors Affecting the Plasma Composition Solute and water content of plasma is affected by movement of materials in and out of the body and by movement of materials between body compartments. Ways in which materials can be gained or lost from plasma: 1. By exchange with cells 2. Exchange with extracellular connective tissue including bone (Ca & P) Outside exchanges: 1. Exchange with materials in the lumen of the GI tract 2. Exchange with materials in the lumen of the kidney tubules 3. Loss through sweating, hemorrhaging and respiration The transport of materials across the wall of the GI tract normally involves a net gain of water and solutes. The transport of materials across the walls of the renal tubules amounts to a net loss of water and solutes by the body. Solute and Water Balance Balance occurs when solutes and water enter and leave the plasma at the same rate. If a substance enters the plasma faster than it leaves and its concentration increases it is in positive balance. If a substance leaves plasma faster than it enters and its concentration decreases it is in negative balance. Certain substances can exist with a negative or positive balance with no change in the plasma concentration when their concentration is controlled by specific regulatory mechanisms. Glucose is an example. In the kidneys 70% of filtered water and sodium is reabsorbed in the proximal convoluted tubules without regulation. The remaining quantity can be reabsorbed depending upon the body's needs. The kidneys can also regulate the potassium, calcium and hydrogen ions that are excreted. Principal cells in the distal convoluted tubules and collecting ducts can adjust water and electrolyte excretion in response to hormonal influence. Intercalated cells in the same location can adjust acid- base balance. Water Balance Water balance is the equality between the water that enters, or is produced in the body, with the water that exits, or is consumed by the body. Only the kidneys regulate the amount of water lost in order to maintain balance. A state of normal blood volume is called normovolemia. When the amount of water taken in exceeds what is lost, the body is in a positive fluid balance and the body becomes hypervolemic. If more water is lost than gained, the body is in a negative fluid balance and the body becomes hypovolemic. Water balance is important because plasma volume affects mean arterial pressure and changes in plasma osmolarity can cause fluid to shift from one body compartment to another and affect cellular functions. Osmolarity and the Movement of Water Kidneys can vary the amount of water lost in the distal convoluted tubules and collecting ducts, but in order to do this, an osmotic gradient needs to be created in the kidney between the lumen of the tubule and the peritubular fluids, and water permeability needs to be regulated. Under normal conditions the various fluid compartments in the body are in osmotic equilibrium with the osmolarity within the cells (intracellular), in between the cells (interstitial fluid) and in the plasma at about 300 mOsmoles. If someone drinks a large quantity of water, the plasma volume expands and its osmolarity decreases. The water moves from the plasma into the interstitial fluid and into the cells because of the osmotic gradient. The movement of water into the cells would cause them to swell. The kidneys correct for this by producing a large quantity of hyposmotic urine. If a person eats a very salty food, the salt is absorbed, enters the plasma and increases plasma osmolarity. Now the water movement is from the cells and interstitial fluid into the plasma and the cells would shrink. The kidneys correct for this by producing a hyperosmotic urine. The kidney adjusts the osmolarity of the urine solely by varying the amount of water reabsorbed by the kidneys. Water reabsorption itself is a passive process that is driven by the osmotic gradients created by the reabsorption of solutes. Water Reabsorption in the Proximal Tubule Sodium is the most abundant solute in the extracellular fluid. The active transport of sodium across the basolateral membrane of the tubular epithelium is primarily responsible for creating the osmotic gradient that causes movement of water. In addition to sodium other solutes are actively reabsorbed contributing to the osmotic gradient that causes water to be reabsorbed. The movement of water from the lumen of the tubule into the plasma brings with it permeant solutes such as urea. Establishment of the Medullary Osmotic Gradient The renal medulla has an osmotic gradient with the interstitial fluid being about 300 mOsmoles near the cortex and increasing in osmolarity up to 1400 mOsmoles towards the tips of the renal pyramids. This gradient is responsible for water reabsorption by the collecting ducts. Countercurrent Multiplier The osmotic gradient is created by the mechanism of the counter current multiplier produced by the loops of Henle of the juxtamedullary nephrons. Study the figure below for an explanation of how the counter current multiplier establishes the medullary osmotic gradient. Urea freely crosses most membranes but in the collecting ducts its movement is facilitated out of the collecting duct and it contributes about 40% to the osmolarity of the gradient. Role of the Vasa Recta The hairpin loops of the capillaries of the vasa recta help to maintain the medullary osmotic gradient because the loss of water and gain of solutes that occurs as the descending limb goes towards the tip of the pyramid is counteracted by the gain in water and loss of solutes as the plasma ascends toward the cortex. Water Reabsorption in the Distal Tubule and Collecting Duct Seventy percent of the filtered water is reabsorbed in the proximal tubule. Of the remaining 30%, 20% is reabsorbed by the distal tubule and 10% by the collecting duct. The reabsorption in the distal part of the tubule results from the fact that the fluid in the lumen of the tubule is always hypo-osmolar compared to the peritubular fluid. The tubular epithelial cells of the late distal tubules and collecting ducts have tight junctions between cells and the cell membranes are relatively impermeable to water. Water is able to pass only through water channels called aquaporins found in the cell membranes. Aquaporin-3 channels are present in the basolateral membrane and aquaporin-2 channels are present in the apical membrane when ADH is present. When the distal tubules and collecting ducts are impermeable to water due to the lack of aquaporins in the apical membrane, the hypo-osmolar fluid entering the tubule remains hypo-osmolar even as it flows through the osmolar gradient created in the medulla and a dilute urine is excreted. When aquaporin-2 channels are present in the apical membrane of these tubules the tubules become permeable to water. The water flows down its osmotic gradient. As the collecting duct descends down the medulla, the peritubular fluid is increasingly hyper-osmotic and continues to draw water from the permeable collecting duct. This continues until the fluid is iso-osmotic to the highly concentrated fluid at the tip of the pyramid which is 1400 mOsmole. This is the most concentrated the fluid can get and the maximum concentrating ability of the kidneys. Hence, in order to rid the body of excess solutes there is always a certain volume of water that is lost (about 440 ml). This is called obligatory water loss. Effects of ADH Antidiuretic hormone or ADH regulates the permeability of the late distal tubules and collecting ducts. ADH stimulates the synthesis of aquaporin-2 and its insertion into the membranes of the principal cells. Therefore, water reabsorption and urine volume are regulated by variations in the plasma levels of ADH. ADH acts by binding to receptors on the plasma membrane. These receptors activate a G protein that activates the enzyme adenylate cyclase which catalyzes the synthesis of cAMP. cAMP causes the following effects: 1. Stimulates insertion of aquaporin-2 into the apical membrane by exocytosis. 2. Stimulates synthesis of aquaporin-2 molecules. Regulation of ADH Secretion Osmoreceptors in the hypothalamus detect changes in osmolarity. When osmolarity increases, ADH is secreted by the pituitary and increases water reabsorption. When osmolarity decreases, ADH secretion is inhibited. Baroreceptors in the atria responding to changes in blood volume, and baroreceptors in the aortic arch and carotid sinus responding to changes in blood pressure also regulate ADH secretion. When blood volume or pressure drop, ADH is secreted which helps to conserve plasma volume by increasing water reabsorption. When blood volume and pressure increases, ADH is inhibited with the opposite effects. A deficiency in ADH secretion causes diabetes insipidus in which there is excessive urination (polyuria) and excessive fluid intake (polydypsia). GFR When blood pressure drops below 80 mm Hg, the GFR can no longer autoregulate and GFR drops. This results in less water being filtered and excreted. When blood pressure is greater than 180 mm Hg the GFR increases. This increases the amount of water that is filtered and then excreted. Sodium Balance Maintaining sodium balance is important for two reasons: 1. It is the primary ion regulating osmolarity of extracellular fluid. As such it is an important determinant of plasma volume and MAP. If sodium levels are high (hypernatremia) there is an increase in blood pressure, hypertension. If sodium levels are low (hyponatremia) there is a decrease in blood pressure, hypotension. 2. Sodium is also an important ion forming the electrochemical gradient of excitable cells. Mechanisms of Sodium Reabsorption In all tubular segments sodium is actively transported. The reabsorption is due to sodium/potassium pumps located in the basolateral membrane of the tubular epithelial cells. The active transport of sodium at the basolateral membrane creates a concentration gradient across the apical membrane favorable for diffusion of sodium into the cell. In the proximal tubule the entry of sodium into the cell is coupled with the movement of other solutes. 1. Sodium enters the cell co-transported with other molecules such as glucose and amino acids. 2. Counter-transported with the hydrogen ion leaving the cell and entering the tubular fluid. In the distal tubule the concentration gradient favoring movement of sodium into the tubular epithelial cell is the same but diffusion of sodium across the apical membrane is: 1. By co-transport with the anions chloride and bicarbonate. 2. Facilitated diffusion through sodium channels. Sodium reabsorption in the distal tubules is often coupled with potassium and hydrogen ions secretion. This helps to minimize changes in the electrical potential across the membrane and facilitates the secretion of potassium and hydrogen ions. Effects of Aldosterone Aldosterone regulates both reabsorption of sodium and secretion of potassium. Aldosterone (a permeant steroid hormone) enters the principal cells of the late distal tubules and collecting ducts and binds to cytosolic receptors. Its effects include: 1. Increasing sodium and potassium channels in the apical membrane by causing channels to open and synthesizing new channels. 2. Increasing synthesis and concentration of Na /K pumps in the basolateral membrane. Both of these effects cause the simultaneous reabsorption of sodium and secretion of potassium. Renin-Angiotensin-Aldosterone System The walls of the afferent arteriole that contributes to the juxtaglomerular apparatus are granular cells that secrete renin. The nearby cells of the macula densa detect changes in the flow, and the sodium and chloride concentration, of the tubular fluid. A decrease in sodium ion concentration causes renin secretion to increase. Renin acts upon angiotensinogen which is secreted by the liver converting it to angiotensin I. Angiotensin converting enzyme (ACE) which is on the surface of the capillary endothelial cells throughout the body, but particularly in the lung, converts angiotensin I to angiotensin II. Angiotensin II increases MAP by the following effects: 1. acts as a vasoconstrictor 2. stimulates release of aldosterone 3. stimulates secretion of ADH 4. stimulates thirst and fluid intake Renin release is stimulated by a decrease in MAP which is specifically detected by: 1. Decrease in afferent arteriole pressure 2. Baroreceptor reflex causing renal sympathetic nerve stimulation 3. A decrease in GFR leading to a decrease in sodium and chloride concentration in the distal tubule Atrial Natriuretic Peptide (ANP) This peptide is secreted by cells of the atrium when an increase in plasma volume causes its walls to stretch. ANP increases sodium excretion by: 1. Increasing glomerular capillary pressure by dilating the afferent arteriole and constricting the efferent arteriole. 2. Decreasing sodium absorption by decreasing the number of open sodium channels in the principal cells. 3. Decreasing secretion of renin and aldosterone. Potassium Balance
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