BSC2086 1st Edition Lecture 22Outline of Last Lecture I. Urinary System FunctionsII. Kidneys III. Renal Tubule IV. Nephron V. Renal Corpuscle VI. Collecting SystemOutline of Current Lecture I. Renal PhysiologyII. Aldosterone and ADHIII. Glomerular FiltrationIV. Reabsorption and SecretionV. Transport, Storage, and Elimination of Urine I. Renal Physiologya. Goal of Producing Urinei. Maintain homeostasis by regulating composition and volume of blood1. Filtrate made by glomerular filtration is concentrateda. Failure to do this will cause too much water loss, or fatal dehydration2. Absorbs and retains materials that are valuable for other tissues, such astissues and amino acids. ii. Includes the excretion of metabolic waste products such as urea, creatinine, uric acid, which are all organic wastes dissolved in the bloodb. Kidneys i. Mostly produce concentrated urineii. 1200-1400 mOsm/L 1. 4x plasma concentrationiii. Expression of osmotic concentration 1. Osmolaritya. Total number of solute particles per literb. Expressed in osmoles per liter (Osm/L) or milliosmoles per liter (mOsm/L)c. The osmotic concentration of body fluids = about 300 mOsm/L2. Large organic molecule concentrationa. Grams or milligrams per unit volume of solution (mg/dL or g/dL)II. Aldosterone and ADHa. Their secretion increases urine osmolarityb. Aldosterone i. Increases the number of Na+/K+ exchange pump at DCT and collecting ductsii. Promotes the reabsorption of Na+ in exchange for K+iii. Water is reabsorbed by osmosisc. ADH i. Increases the aquaporins, or water channels, in apical cell membranes of DCT and collecting ductii. Concentrates 100 mOsm/L tubular fluid arriving at DCT to be concentrated to 1200 mOsm/L when it reaches the minor calyxd. Absence of ADHi. All fluid arriving at DCT is lost in urine since water is not reabsorbedii. As seen in diabetes insipidus, large amounts of dilute (20-400 mOsm/L) urine (24L/day)iii. Post. Pit. Normally is continuously secreting low levels of ADH1. DCT and collecting system are both always permeable to water2. Collecting system reabsorbs 16.8 L/day (9.3% of filtrate) 3. produces 1200 mL per day (0.6% of filtrate) of urine (800–1000 mOsm/L)III. Glomerular Filtration a. Governed by the balance between:i. Hydrostatic pressure 1. Fluid pressure2. Blood pressure in glomerular capillaries3. Usually pushes water and solutes out of plasma and into filtrate4. Significantly higher than capillary pressures in the systemic circuit a. This is due to the arrangement of vessels at the glomerulus b. Blood leaving glomerular capillaries will flow into an efferent arteriolec. Efferent arteriole has a small diameter than an efferent arteriole, therefore producing more resistance and requiring a relatively high pressure to force blood into itii. Colloid osmotic pressure on both sides of capillary walls1. Pressure of materials in solution trying to draw fluid inb. Capsular hydrostatic pressure (CsHP)i. Fluid stuck inside the capsule that opposes glomerular hydrostatic pressureii. Pushes water and solutes out of filtrate and into plasmaiii. A result of the resistance to flow along nephron and conducting systemiv. 15 mmHg average c. Net hydrostatic pressure (NHP)i. Glomerular hydrostatic pressure – capsular hydrostatic pressured. Colloid osmotic pressure i. Osmotic pressure due to suspended proteins ii. Blood colloid osmotic pressure (BCOP)1. Draws water out of filtrate and into plasma, thus opposing filtration2. 25 mmHg average e. Net filtration pressure (NFP)i. Average pressure that forces water and dissolved materials out of glomerular capillaries and into the capsular spaceii. At glomerulus, it accounts for the difference between hydrostatic pressure and BCOP across the glomerular capillariesiii. NFP – (GHP-CsHP) – BCOP1. Should never be negative2. If zero, then no filtration is occurringf. Glomerular filtration rate (GFR)i. Amount of filtrate produced by kidneys each minuteii. 10% of fluid delivered to kidneys1. Leaves the bloodstream and enters capsular spaces2. Averages about 125 mL/min at each kidneyiii. About 48 gallons of filtrate are made by the glomeruli per day1. 99% is reabsorbed in the renal tubules iv. Control1. Autoregulation a. Local levelb. Maintains GFR regardless of changes in local blood pressure andblood flow c. Changes the diameters of afferent arterioles, efferent arterioles, and glomerular capillaries d. Reduced blood flow or glomerular blood pressure causes: i. Dilation of glomerular capillaries and afferent arterioleii. Constriction of efferent arteriole 1. This increased resistance as blood is flowing out will increase the pressure in the glomerulus e. Rise in renal blood pressure:i. Stretches walls of afferent arterioles ii. Smooth muscle cells contract and constrict afferent arterioles iii. Hydrostatic pressure drops, less filtration 2. Hormonal regulationa. Initiated by kidneys b. Renin-angiotensin systemi. Increases GFP by constricting efferent arterioleii. Stimulates aldosterone release by the adrenal cortex and ADH by the posterior pituitary and Na+ and H2O reabsorption iii. Increases thirstiv. Increases sympathetic motor tone, cardiac output, and vasoconstriction of arterioles and precapillary sphincters 1. Try to increase blood pressure and blood volumev. Natriuretic peptides (ANP and BNP)1. Released by heart when there is too much fluid in it2. Dilates the afferent arteriole and constricts efferent arteriole3. Increases GFP and GFR 4. Makes more urine, decreases blood volume 3. Autonomic regulation a. Sympathetic division of ANSb. Consists mostly of sympathetic preganglionic fibersc. Activation of sympathetic nervous system:i. Constricts afferent arteriolesii. Decreases GFR which slows filtrate productiond. Sympathetic stimulation also changes blood flow to the kidneys i. Can be opposed by autoregulation at a local level IV. Reabsorption and Secretiona. Control of blood pH which is crucial to homeostasisi. Removal of H+ii. Bicarbonate production b. Acidosis i. Lactic acidosis develops after exhaustive muscle activityii. Ketoacidosis develops during starvation or diabetes mellitus c. Alkalosis i. Abnormally high blood pH1. May be caused by prolonged stimulation of aldosterone2. Stimulates secretion of H+ and loss of H+ in urine d. Vasa rectai. Made by peritubular capillaries of juxtamedullary nephronsii. Functions:1. Return the water and solutes reabsorbed in the medulla to general circulation without disrupting the concentration gradienta.
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