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Unit 4 - Fluid and Electrolyte Balance - Full Textbook Notes

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BIOL 373
Heidi Engelhardt

Chapter 20: Integrative Phys II – Fluid and Electrolyte Balance The homeostatic control and mechanisms for fluid and electrolyte balance in the body are aimed at maintaining four parameters: 1. Fluid volume 2. Osmolarity 3. The concentration of individual ions 4. pH Fluid and Electrolyte Homeostasis  the body’s task is to maintain mass balance: what comes in must be excreted if the body does not need it  water and ions can be excreted via the kidneys, feces, sweat, and lungs  water and sodium are associated with extracellular fluid volume and osmolarity  water will move in or out of a cell if the osmolarity of ECF fluid changes, which inturn changes the intracellular volume o ECF osmolarity ↓ (as a result of excess water intake), water moves into the cells and they swell o ECF osmolarity ↑ (as a result of salt intake), water moves out of the cells and they shrink 1. Some cells can maintain their volume by synthesizing organic solutes as needed to make their intracellular osmolarity match that of the interstitial fluid o These solutes include sugar alcohols and certain amino acids 2. Other cells regulate their volume by changing their ionic composition  Changes in cell volume can initiate certain cellular responses o Swelling liver cells activates protein and glycogen synthesis and shrinking causes the breakdown  Fluid and electrolyte balance involves the respiratory and cardiovascular systems, as well as the renal and behavioural responses o Lungs and cardiovascular are controlled through neural pathways  changes occur quickly o Kidneys are controlled by the endocrine and neuro-endocrine control  changes occur more slowly  Behavioural Pathway: Low blood pressure (volume receptors in atria and carotid and aortic baroreceptors)  elicits thirst causing water uptake  ECF and ICF volume increases  Cardiovascular system: low blood pressure (volume receptors in atria and carotid and aortic baroreceptors)  cardiac output increases, causing vasoconstriction  blood pressure increases  Cardiovascular system: high blood pressure (volume receptors in atria and endocrine cells in atria, and carotid and aortic baroreceptors)  cardiac output decreases, causing vasodilation  blood pressure decreases  Kidney Pathway: low blood pressure (volume receptors in atria and carotid and aortic baroreceptors)  conserve water to minimize further volume loss  blood pressure increases  Kidney Pathway: high blood pressure (volume receptors in atria and endocrine cells in atria, and carotid and aortic baroreceptors)  excretes salts and water in urine  ECF and ICF volume decreases  blood pressure decreases Water Balance  The most abundant molecule in the body: 50% of females and 60% of males (age 17-39)  67% of water is inside cells, 7% is in the plasma, and 26% is in the interstitial fluid  Intake MUST EQUAL output  On average an adult will ingest a little more than 2 liters of water in food and drink in a day +.3 liters of water from metabolism (aerobic respiration) = ~2.5 liters  Most water is lost in the urine (~1.5 liters) and a small portion is lost in feces o only water loss in urine can be monitored o urine is normally the major route of water loss (exceptions include excessive sweating, diarrhea,  Insensible water loss: we are not normally aware of it; it occurs across the skin surface and through exhalation of humidified air; we lose about 900mL of water each day  Kidneys o Volume lost to the environment must be replaced from the environment o The kidneys cannot replenish lost water, all they can do is conserve it o If the kidneys need to conserve water, the urine becomes quite concentrated o Specialized mechanisms in the medulla of the kidney allow urine to be up to 4 times as concentrated as the blood o Urine concentration is controlled by varying the amounts of water and Na+ reabsorbed in the distal nephron o Diuresis: the removal of excess water in urine; drugs that promote the excretion of urine are called diuretics o Dilute urine is produced when the kidney reabsorbs solutes without allowing water to follow by osmosis  The apical tubule cell membranes must not be permeable to water  If urine is to become concentrated, then the nephron must be able to reabsorb water but leave solute in the tubule lumen  The collecting duct cells and interstitial fluid surrounding them must be made more concentrated than the fluid flowing into the tubule  Then water can be absorbed from the lumen without first reabsorbing solute  The renal medulla maintains a high osmotic concentration in its cells and interstitial fluid which allows urine to be concentrated as it flows through the collecting duct  Renal cortex osmolarity = 300 mOsM o Water is reabsorbed only by osmosis through water pores (or aquaporins)  Aquaporins are a family of membrane chanels with at least 10 different isoforms that occur in mammalian tissue  The kidney has multiple isoforms, including Aquaporin-2 (AQP2)  4 steps of osmolarity changes through the nephron 1. Isosmotic fluid leaving the proximal tubule becomes progressively more concentrated in the descending limb  Fluid entering the loop of henle is ~300 mOsM  As the nephrons get lower in the medulla, the concentration increases until it reaches a maximum of ~1200 mOsM where the collecting ducts empty into the renal pelvis 2. Removal of solute in the thick ascending limb creates hyposmotic fluid  The permeability of the tubule wall changes in the ascending limb of the nephron  The cells in the thick portion of the ascending limb have apical surface (facing the tubule lumen) that are impermeable to water> these cells transport ions out of the tubule lumen but solute movement will not be followed by osmosis  This decreases the concentration of the tubule (less solutes to lots of water; more diluted concentration)  Osmolarity is around 100 mOsM  The loops of Henle is the primary site where the kidney creates hyposomatic fluid 3. Permeability to water and solutes is regulated by hormones  Water permeability of the tubule cells is variable and under hormonal control  When the apical membrane is impermeable to water, water cannot leave the tubule, and the filtrate remains dilute  OR if the body needs to conserve water, the tubule epithelium in the distal nephron must become permeable to water> under hormonal control, the cells insert water pores into their apical membranes  Osmosis draws water out of the less concentrated lumen and into the more concentrated interstitial fluid 4. Urine osmolarity depends on reabsorption in the collecting duct  A small amount of solute can be absorbed as fluid passes along the collecting duct, making the filtrate even more dilute  The concentration of urine can be as low as 50 mOsM and as high as 1200 mOsM  Only the ingestion or infusion of water can replace water that has been lost!  Vasa Recta are the capillaries  Vasopressin (Antidiuretic Hormone; ADH): posterior pituitary hormone that regulates water reabsorption in the kidney o 9 amino acid peptide that contains the amino acid arginine > AKA arginine vasopressin or AVP o Causes the target cells of the collecting duct epithlium to become permeable to water, allowing water to move out of the lumen o The water moves by osmosis because solute concentration in the cells and interstitial fluid of the renal medulla is higher than that of fluid in the tubule o In the absence of vasopressin, the collecting duct is impermeable to water o Permeability is variable, depending on how much vasopressin is present o Regulates Aquaporin-2 (AQP2)  May be found in two locations: on the apical membrane facing the tubule lumen and in membrane of cytoplasmic storage vesicles  When vasopressin levels and water permeability in the collecting duct are both low, the collecting duct cells have a few water pores in its apical membrane and stores its AQP2 water pores in cytoplasmic storage vesicles  Vasopressin arrives at the collecting duct  binds to V2 receptors on the basolateral side of the cell  G-protein/cAMP second messenger system is activated  Intracellular proteins are phosphorylated  AQP2 vesicles move to the apical membrane and fuse with it  exocytosis inserts the AQP2 water pores into the apical membrane  Water is absorbed by osmosis into the blood  Membrane recycling: the process in which parts of the cell membrane are alternately added by exocytosis and withdrawn by endocytosis  3 stimuli that control plasma vasopressin secretion: 1. Plasma osmolarity > an increase in plasma osmolarity is the most potent stimulus  Monitored by osmoreceptors, stretch-sensitive neurons that increase their firing rate as osmolarity increases  If osmoreceptors shrink, cation channels linked to actin filaments open, depolarizing the cell  The primary osmoreceptors for vasopressin are found in the hypothalamus > if plasma osmolarity is below 280 mOsM then osmoreceptors do not fire, and vasopressin release is stopped > if it is above 280 mOsM, then the osmoreceptors stimulate the release of vasopressin 2. Blood volume > less powerful than plasma osmolarity  Primary receptors for decreases volume are stretch-sensitive receptors in the atria  If low, it signals the hypothalamus to secrete vasopressin and conserve fluid 3. Blood pressure> less powerful than plasma osmolarity  Monitored by the same carotid and aortic barorecpetors that initiate cardiovascular responses  If low, it signals the hypothalamus to secrete vasopressin and conserve fluid  Vasopressin in adults shows a circadian rhythm, with increases secretion during the overnight hours o Less urine is produced overnight than during the day, and the first urine excreted in the morning is more concentrated  Nocturnal enuresis (bed-wetting): one theory for the cause is that these children have a developmental delay in the normal pattern of increases vasopressin secretion at night o With less vasopressin, the children’s urine output stays elevated, causing the bladder to fill to its maximum capacity and empty spontaneously during sleep o Can be treated with the nasal spray: desmopressin  Vasopressin is made and packaged in the cell body of neurons in the hypothalamus  vesicles are transported down the cell  vesicles containing AVP are stored in posterior pituitary  AVP is released into blood and dissolved in plasma o Has a half-life of 15 minutes  The kidney’s ability to produce concentrated urine is the high osmolarity of the medullary intersitium (intersitial fluid compartment of the kidney) o Without it, there would be no concentration gradient for osmotic movement of water out of the collecting duct  Countercurrent exchange systems: require arterial and venous blood vessels that pass very close to each other, with their fluid flow moving in opposite directions o Allows the passive transfer of heat or molecules from one vessel to the other o The kidney forms a closed system, the solutes are not lost to the environment, and instead they concentrate in the interstitium  This process is aided by active transport of solutes out of the ascending limb of the loop of Henle, which makes the ECP osmolarity even greater o Countercurrent Multiplier: a countercurrent exchange system in which the exchange is enhanced by active transport of solutes o The Renal Countercurrent Multiplier  Two components: loops of Henle that leave the cortex, dip down into the more concentrated environment of the medulla, then ascend into the cortex again, and the pertubular capillaries known as the vasa recta  Vase recta capillaries dip down into the medulla and then go back up to the cortex, also forming hairpin loops that act as a countercurrent exchanger  blood flow in the vasa recta moves in the opposite direction from filtrate flow in the loops of Henle  [pathway : isomotic filtrate from the proximal tubule flows into the descending limb of the loops of Henle  the descending limb is permeable to water but does not transport ions; as the loops dips into the medulla, water moves by osmosis from the descending limb into the progressively more concentrated interstitial fluid, leaving solutes behind the tubule lumen  the filtrate becomes progressively more concentrated as it moves deeper into the medulla  as the tops of the longest loops of Henle, the filtrate reaches a concentration of 1200 mOsM  filtrate shorter loops (which do not extend into the most concentrated regions of the medulla) does not reach such a high concentration  when the fluid flow reverses direction and enters the ascending limb of the loops, the properties of the tubule epithelium change; the tubule epithelium in this segment of the nephron is impermeable to water while actively transporting Na+, K+ and Cl- out of the tubule into the interstitial fluid  the loss of solute from the lumen causes the filtrate osmolarity to decreases steadily, from 1200 mOsM at the bottom of the loop to 100 mOsM at the point where the ascending limb leaves the medulla and enters the cortex ]  the net result of the countercurrent multiplier in the kidney is to produce hyperosmotic interstitial fluid in the medulla, and hyposmotic filtrate leaving the loop of Henle  ~25% of all Na+ and K+ reabsorption takes place in the ascending limb of the loop  NKCC symporter transporter uses energy stored in the Na+ concentration gradient to transport Na+, K+ and 2 Cl- from the lumen into the epithelium cells of the ascending limb  NKCC-mediated transport can be inhibited by drugs known as “loop diuretics” such as furosemide (Lasix)  Na+-K+-ATPase removes Na+ from the cells on the basolateral side of the epithelium, while K+ and Cl- leave the cells together on a cotransport protein or through open channels  water or solutes that leave the tubule move into the vasa recta if an osmotic or concentration gradient exists between the medullary interstitium and the blood in the vasa recta o as blood flows deeper into the medulla, it loses water and picks up solutes transported out of the ascending limb of the loop of Henle, carrying these solutes farther into the medulla o by the time the blood reaches the bottom of the vasa recta loop, it has a high osmolarity, similar to that of the surrounding interstitial fluid (1200 mOsM) o as blood flows back toward the cortex, the high plasma osmolarity attracts the water that is being lost from the descending limb o as water moves back into the vasa recta, the osmolarity of the blood decreases while simultaneously preventing the water from diluting the concentrated medullary interstitial fluid o without the vasa recta, the water from the loop of Henle would eventually dilute the medullary interstitium  more than half the solutes in the medullary interstitium is urea o membrane transporters for urea are present in the collecting duct and loops of Henle  consist of facilitated diffusion carriers, and Na+ dependent secondary active transporters > these transporters help concentrate urea in the medullary interstitium, where it contributes to the high interstitial osmolarity Sodium Balance and ECF Volume  we ingest ~9 grams of salt a day  salt increases osmolarity which triggers two responses: o vasopressin secretion > causes the kidneys to conserve water (by reabsorbing water from the filtrate) and concentrate the urine o thirst > prompts us to drink water or other fluids  the increases fluid intake increases both ECF volume and blood pressure  triggers other control pathways which bring everything back to normal by excreting extra salt and water  The kidneys are responsible for most sodium excretion, and normally only a small amount of sodium leaves via feces and perspiration  Only renal sodium absorption is regulated  Sodium balance pathways are stimulated more by blood volume and blood pressure than sodium levels themselves; chloride movement usually follows sodium movement either through an electrochemical gradient, NKCC transporters or the Na+-Cl- symporter  Aldosterone: a steroid hormone that stimulates Na+ reabsorption and K+ secretion in the kidney o Increases Na+-K+-ATPase activity o The more aldosterone, the more Na+ reabsorption o Synthesized in the adrenal cortex, the outer portion of the adrenal gland that sits atop each kidney> secreted into the blood and transported on a protein carrier to its target o Aldosterone acts in the last 3 of the distal tubule and the portion of the collecting duct that runs through the kidney cortex o Targets Principal cells (P cells)  P cells are arranged like other polarized transporting epithelial cells, with Na+-K+-ATPase pumps on the basolateral membrane, and various channels and transporters on the apical membrane  The apical membrane contains leak channels for sodium, called ENaC (Epithelial Na+ Channel), and for K+, called ROMK (renal outer medulla K+ channel)  Aldosterone enters P cells by diffusion 1. Aldosterone combines with a cytoplasmic receptor (cytosolic mineralocorticoid (MR) receptor) inside the P cell o In the early response phase, apical Na+ and K+ channels increase their open time under the influence of an as-yet-unidentified signal molecule o Intracellular Na+ levels rise, the Na+-K+-ATPase pump speeds up, transporting cytoplasmic Na+ into the ECF and bringing K+ from the ECF into the P cell; results in a rapid increase in Na+ reabsorption and K+ secretion that does not require the synthesis of new channel or ATPase proteins 2. Hormone-receptor complex initiates transcription in the nucleus 3. Translation and protein synthesis makes new protein channels and pumps o They are inserted into epithelial cell membranes 4. Aldosterone-induced proteins modulate existing channels and pumps 5. Result is increased Na+ reabsorption and K+ secretion o Sodium and Water reabsorption are separately regulated in the distal nephron o Water does not follow Na+ reabsorption; vasopressin must be present to make the cell walls permeable to water o However, Na+ reabsorption is always followed by osmosis in the proximal tubule epithelium since it is always permeable to water o 50-70% bound to plasma protein o Half-life is 15 minutes o Natriuretic peptides inhibit release of aldosterone  There are two primary stimuli of aldosterone secretion: o increased extracellular K+ concentration> act directly on the adrenal cortex in a reflex that protects that body from hyperkalemia o decreased blood pressure> initiates a complex pathway that results in released of a hormone, Angiotensin II, that stimulates aldosterone secretion in most situations o two additional factors modulate aldosterone release in pathological states:  an increase in ECF osmolarity acts directly on adrenal cortex cells to inhibit aldosterone secretion during dehydration  an abnormally large (10-20mEq/L) decrease in plasma Na+ can directly stimulate aldosterone secretion  Angiotensin II (ANG II) o The usual signal controlling aldosterone release from the adrenal cortex o One component of the renin-angiotensin system (RAS), a complex, multistep pathway for maintaining blood pressure  RAS pathway begins with juxtaglomerular granular cells in the afferent arterioles of a nephron, secrete an enzyme called renin  Renin converts an inactive plasma protein, angiotensinogen, into angiotensin I (ANG I)  When ANG I encounters an enzyme called angiotensin-converting enzyme (ACE), ANG I is converted to ANG II > occurs throughout the body  Stimuli of the RAS pathway:  The granular cells are directly sensitive to blood pressure; they respond to low BP in renal arterioles by secreting renin  Sympathetic neurons, activated by the cardiovascular control center when blood pressure decreases, terminate on the granular cells and stimulate renin secretion  Paracrine Feedback – from the macula densa in the distal tubule to the granular cells – stimulates renin release; when fluid flow through the distal tubule is relatively high, the macula densa cells release paracrines, which inhibit renin release; when fluid flow in the distal tubule decreases, macula densa cells signal the granular cells to secrete renin o When ANG II in the blood reaches the adrenal gland, it causes synthesis and release of aldosterone o At the distal nephron, aldosterone initiates intracellular reactions that cause the tubule to reabsorb NA+ o Sodium does not directly raise low BP, but retention of Sodium increases osmolarity, which stimulates thirst fluid intake causes an increase in ECF volume; when blood volume increases so does BP o Increases blood pressure both directly and indirectly through 4 additional pathways: 1. ANG II increases vasopressin secretion> ANG II receptors in the hypothalamus initiate this reflex; fluid retention in the kidney under the influence of vasopressin helps conserve blood volume, thereby maintaining blood pressure 2. ANG II stimulates thirst> fluid ingestion is a behavioural response that expands blood volume and raises blood pressure 3. ANG II is one of the most potent vasoconstrictors known in humans> vasoconstriction causes blood pressure to increase without a change in blood volume 4. Activation of ANG II receptors in the cardiovascular control center increases sympathetic output to the heart and blood vessels > sympathetic stimulation increases cardiac output and vasoconstriction, both of which increase blood pressure 5. ANG II increases proximal tubule Na+ reabsorption> ANG II stimulates an apical transporter, the Na+-H+ exchanger (NHE); sodium reabsorption in the proximal tubule is followed by water reabsorption, so the net effect is reabsorption of isosmotic fluid, conserving volume o ACE inhibitors block the ACE-mediated conversion of ANG I to ANG II, thereby helping to relax blood vessels and lower BP > less ANG II means less aldosterone release, a decrease in Na+ reabsorption and ultimately a decrease in ECF volume  ACE inactivates a cytokine called bradykinin; when ACE is inhibited, bradykinin levels increase, and in some patients this creates a dry, hacking cough o Angiotensin Receptor Blockers (ARBs): block the BP-raising effects of ANG II at target cells by binding to AT1 receptors o Direct renin inhibitors decrease the plasma activity of renin, which in turn blocks production of ANG I and inhibits the entire RAS pathway o 8 amino-acid peptide o → → o Angiotensin is dissolved in plasma o Half life is 1 minute; renin half life is 10-20 minutes o Effects the adrenal cortex (secretes aldosterone), arterioles (vasoconstriction), medulla oblongata(reflexes to increase BP), and hypothalamus (vasopressin secretion and increased thirst)  Natriuresis: sodium loss in urine  Diuresis: water loss in the urine  Atrial Natriuretic peptide (ANP): a peptide hormone produced in specialized myocardial cells primarily in the atria of the heart o Synthesized as part of a large prohoromone that is cleaved into several active hormone fragments o More important signal molecule o Is released when increased blood volume causes increased atrial stretch o Enhances Na+ and water excretion to decrease blood volume o Causes GFR in the kidney by dilating the afferent arterioles, and it directly decreases Na+ reabsorption in the collecting duct o 28 amino acids o Half-life is 2-3 minutes  Brain natriuretic peptide (BNP): synthesized by ventricular myocardial cells and certain brain neurons o Recognized as an important marker for heart failure because production of this substance increases with ventricular dilation and increased ventricular pressure o BNP levels are used to predict heart failure and sudden death from cardiac arrhythmias o 32 amino acids o Half-life is 12 minutes  When myocardial cells stretch more than normal, both ANP and BNP are released by the heart o They bind to membrane receptor-enzymes that work through a cGMP second messenger system o Act to increase sodium and water excretion by suppressing the release of renin, aldosterone, and vasopressin o Act on the medulla to lower blood pressure o Dissolved in plasma Potassium Balance  If intake exceeds excretion and plasma K+ goes up, aldosterone is released into the blood through the direct effect of hyperkalemia on the adrenal cortex  aldosterone acting on distal-nephron P cells keeps the cells’ apical ion channels open longer and speed up the Na+- K+-ATPase pump, enhancing renal excretion of K+  changes in extracellular K+ concentration affect the resting membrane potential of all cells  If plasma and ECF K+ concentration decrease (hypokalemia), the concentration gradient between the cell and the ECF becomes larger, more K+ leaves the cell, and the resting membrane potential becomes more negative  If ECF K+ concentrations increase (hyperkalemia), the concentration gradient decreases and more K+ remains in the cell, depolarizing it  When plasma K+ concentrations change, anions such as Cl- are also added to or subtracted from the ECF at a 1:1
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