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126 Cards in this Set
- Front
- Back
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Summary of Kidney Functions
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Excretion of metabolic waste products: urea, creatinine, bilirubin, hydrogen
Excretion of foreign chemicals: drugs, toxins, pesticides, food additives Secretion, metabolism, and excretion of hormones renal erythropoetic factor 1,25 dihydroxycholecalciferol (Vitamin D) Renin Regulation of acid-base balance Gluconeogenesis: glucose synthesis from amino acids Control of arterial pressure Regulation of water & electrolyte excretion Main job of kidney is to excrete urea which is the by product of protein metabolism 2nd job is to maintain acid base balance, then water/salt balance |
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Capsule has reticular tissue-no stretch-maintains________ hydrostatic pressure
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high
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functional unit of the kidney
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Nephron:
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tissue at Bottom of henle is ?
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squamous
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Prox has _________, none on distal
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villi (BRUSH border)
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Juice goes out through ______ into bowmans’ capsule
Renin adjusted by ? |
podocytes
juxta-aparatuys |
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Incr symp activity will _______ GFR
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drop
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GFR is
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how much juice gets pushed through the podocytes per minute
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regulation of GFR
sympathetic nerves afferent arteriole? GFR? |
baroreceptors/higher brain centers
constricts decresases |
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regulation of GFR
low BP afferent arteriole? GFR? |
dilates
no change |
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regulation of GFR
increased BP afferent arteriole? GFR? |
constricts
no change |
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Proximal convoluted tubular cells –
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can actively transport molecules from filtrate back into blood. By reabsorption
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protien
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not filtered
sam % in renal artery zero clearnace |
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insulin
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filtered, not reabsorbed or secreted
less % than in renal artery clearance = to GFR |
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urea
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filtered partially reabsorbed
less % than in renal artery clearance less than GFR |
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glucose
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filtered completely reabsorbed
% = renal artery zero clearance |
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PAH
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filtered and secreted
% less than RA, (appraches zero) clearance graeter than GFR (up to total plasma flow rate) |
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K
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filtered, reabsorbed and secreted
variable % in renal vein variable clearance |
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Excretion of Metabolic Waste Products
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Urea (from protein metabolism)
Uric acid (from nucleic acid metabolism) Creatinine (from muscle metabolism) Bilirubin (from hemoglobin metabolism) |
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Excretion of Chemicals
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Pesticides
Food additives Toxins Drugs |
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Secretion, Metabolism,
and Excretion of Hormones Hormones produced in the kidney |
Renal erythropoetic factor
1,25 dihydroxycholecalciferol (Vitamin D) Renin |
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Secretion, Metabolism,
and Excretion of Hormones metabolized and excreted by the kidney |
Most peptide hormones (e.g., insulin, angiotensin II, a zillion of ‘em.)
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Counter current multiplier
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Pumping out of NaCl out of the ascending limb makes the interstitium more conc.
Vasa recta pick up salt Salt is actively pumped out |
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Urea keeps the filtrate concentrated in the distal tubule
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Water is pulled back into the filtrate because of high concentrations of urea
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proximal tubule-active transport?
passive? |
na
Cl- ,water,urea |
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descending loop of henle
active transport? passive? |
none
maybe na, water, no urea |
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Thin segment of ascending limb
active transport? passive? |
no active
nacl, no water, urea |
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Thick segment of ascending limb
active transport? passive? |
na
cl-, no water, no urea |
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distal tubule
active transport? passive? |
na
cl-, no water (exc ept the lat part of tubule), no urea |
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collectin duct (dep[ends on adh_)
active transport? passive? |
slight na
no salt, water (adh) or slight with no ADH, urea |
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ADH secretion and action
increased osmolality (dehydration) osm rec's in hypothalamus |
increased ADH
decreased urine volume increased water retention decreased blood osmolality |
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ADH secretion and action
decreased osmolality osm rec's in hypothalamus |
decreased ADH
water loss (increased urine volume) increased blood osm |
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ADH secretion and action
increased blood volume stretch receptors in left atrium |
decreased ADH
increased urine volume decreased blood volume |
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ADH secretion and action
decreased blood volume stretch receptors in left atrium |
increased ADH
decreased urine vol increased blood volume |
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adh from?
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poterior pituitary
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Secretion is
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the active transport of molecules from the peritubular cap.s into the filtrate
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Inulin –
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a polysaccharide produced by onions, artichokes and garlic – is not reabsorbed or secreted. It’s a good indicator of renal clearance and GFR
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PAH = para-aminohippuric acid
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PAH is both filtered and secreted
It is a good measure of renal blood flow |
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Excretion = Filtration –
Reabsorption + Secretion |
Filtration: somewhat variable, not selective (except for proteins), averages 20% of renal plasma flow
Reabsorption: highly variable and selective, most electrolytes (e.g. Na+, K+, Cl-) and nutritional substances (e.g. glucose) are almost completely reabsorbed; most waste products (e.g. urea) poorly reabsorbed Secretion: variable; important for rapidly excreting some waste products (e.g. H+), foreign substances (including drugs), and toxins |
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The reabsorption of Na+ and the secretion of K+ and H+ in the distal tubule. High H+ conc in the blood can lower secretion of K+ (K+ will be lost in the urine)
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You lose K if you are acidotic
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when a substance is secreted by the nephron, it's renal plasma clearance is ________ than the GFR
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greater
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Glomerular Filtration
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GFR = 125 ml/min = 180 liters/day
Plasma volume is filtered 60 times per day Glomerular filtrate composition is about the same as plasma, except for large proteins Filtration fraction (GFR/Renal Plasma Flow) = 0.2 (i.e., 20% of plasma is filtered) |
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Glomerular Capillary Membrane Filtration Barrier
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Endothelium (fenestrated, 160-180 A pores)
Basement Membrane (70-80 A pores), negative charged proteoglycans, restriction site for proteins Epithelial Cells (podocytes, 80-80 A pores) restriction site for proteins |
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Glomerular Capillary Filtration
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Normally not highly variable
Disease that can reduce Kf (filtration constant) and GFR chronic hypertension obesity / diabetes mellitus glomerulonephritis Atg/antibodies can get lodges in the glomerulus….like lupus, arthritic conditions |
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The Ability of a Solute to Penetrate the
Glomerular Membrane Depends on: |
Molecular size ( small molecules > filterability)
Ionic charge (cations > filterability) |
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Bowman’s Capsule Hydrostatic Pressure (PB)
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Normally changes as a function of GFR, not a physiological regulator of GFR
Tubular Obstruction kidney stones tubular necrosis Urinary tract obstruction Prostate hypertrophy/cancer |
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Glomerular Hydrostatic Pressure (PG)
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Is the determinant of GFR most subject to
physiological control? Factors that influence PG: arterial pressure (effect is buffered by autoregulation) afferent arteriolar resistance efferent arteriolar resistance |
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Regulation of Arterial Pressure
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Endocrine Organ
renin-angiotensin system prostaglandins kallikrein-kinin system Control of Extracellular Fluid Volume |
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regulation of renin and aldosterone secretion
decreased blood volume |
increased renin
increased AT-2 increased aldosterone low blood volume stimulates renal baroreceptorsa, granular cells release renin |
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regulation of renin and aldosterone secretion
increased blood volume |
decreased renin
decreased AT-2 decreased aldosterone increased blood volume inhibits baroreceptors. increased NA in distule tubule acts via macula densa to inhibit renin release |
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regulation of renin and aldosterone secretion
increased K+ |
no effect on renin
no effect on AT-2 increased aldosterone direct stimulation of adrenal cortex |
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Regulation of Arterial Pressure
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Endocrine Organ
renin-angiotensin system prostaglandins kallikrein-kinin system Control of Extracellular Fluid Volume |
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regulation of renin and aldosterone secretion
decreased blood volume |
increased renin
increased AT-2 increased aldosterone low blood volume stimulates renal baroreceptorsa, granular cells release renin |
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regulation of renin and aldosterone secretion
increased blood volume |
decreased renin
decreased AT-2 decreased aldosterone increased blood volume inhibits baroreceptors. increased NA in distule tubule acts via macula densa to inhibit renin release |
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regulation of renin and aldosterone secretion
increased K+ |
no effect on renin
no effect on AT-2 increased aldosterone direct stimulation of adrenal cortex |
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Diuretics
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Work on different parts of the nephron to promote the excretion of water.
Electrolytes can leave with the water – that may be bad. |
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Other Factors That Influence GFR
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Prostaglandins: increase GFR; non-steroidal
anti-inflammatory agents can decrease GFR, especially in volume depleted states Fever, pyrogens: increase GFR Glucorticoids: increase GFR Aging: decreases GFR ~10%/decade after 40 yrs Dietary protein: high protein increases GFR low protein decreases GFR Hyperglycemia: increases GFR (diabetes mellitus) |
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loop diretics
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inhibit na transport
thick segments of scending limbs |
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thiazides
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inhibit na transport
last part of ascending limb and first part of distal |
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carbonic anhtdrase inhi8bitors
acetazolamide |
inhibit reabsorption of bicarb
prox tubule |
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osmotic diretics
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reduces osmotic reabsorption of water by reducing gradient
last part of distal tubule and cortical collecting duct |
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K-sparing
spironolactone |
inhibits na reabsorbtion and K secretion
last part of distal tubule and cortical collecting duct |
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Functions of Renal Blood Flow
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To deliver enough plasma to kidneys for
glomerular filtration To deliver nutrients to kidney so that the renal cells can perform their functions (only about 20% of renal blood flow needed for this function) |
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Regulation of Erythrocyte Production
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by kidneys
increased o2 delivery to bean increases EPO which increased RBC production in marrow |
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Regulation of Vitamin D Activity
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by kidney
Kidney produces active form of vitamin D (1,25 dihydroxy vitamin D3 ) Vitamin D3 is important in calcium and phosphate metabolism |
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Regulation of Acid-Base Balance – along with lungs
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Excrete acids (kidneys are the only means
of excreting non-volatile acids) Regulate body fluid buffers ( e.g. Bicarbonate) Acidification of the urine |
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Glucose Synthesis
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Gluconeogenesis: kidneys synthesize glucose
from precursors (e.g., amino acids) during prolonged fasting |
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Clinical Significance of Proteinuria
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Early detection of renal disease in at-risk patients
hypertension: hypertensive renal disease diabetes: diabetic nephropathy pregnancy: gestational proteinuric hypertension (pre-eclampsia) annual “check-up”: renal disease can be silent Assessment and monitoring of known renal disease “Is the dipstick OK?”: dipstick protein tests are not very sensitive and not accurate: “trace” results can be normal & positives must be confirmed by quantitative laboratory test. |
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Microalbuminuria
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Definition: urine excretion of > 25-30 but < 150mg albumin per day
Causes: early diabetes, hypertension, glomerular hyperfiltration Prognostic Value: diabetic patients with microalbuminuria are 10-20 fold more likely to develop persistent proteinuria |
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Three renal processes
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Glomerular filtration
Tubular resorption Tubular secretion |
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Glomerular filtration
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Glomerular membrane is more than 100X more permeable than capillaries elsewhere.
Hydrostaic pressure is the main filtration pressure The most prominent factor in changing GFR is hydrostatic pressure. Kidneys receive 20% - 25% of C.O. |
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Prox Conv Tube and descending Henle’s
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65% of filtrate is reabsorbed through PCT walls back into body. Molecules and water.
Filtrate remains isosmotic- tube is permeable to water Reabsorption occurs constantly, regardless of hydration level. 20% more is reabsorbed constantly, by the descending Henle loop PCT and descending Henle’s unaffected by hormones – ADH and aldosterone 6% of total body energy is given over to reabsorption The remaining 15% of the filtrate (which would amount to 27 L/day) has to be further reduced in ascending Henle’s, DCT, and collecting ducts to maintain body fluid A person with normal hydration produces 1.5L/day of urine. 99.2% of the ultrafiltrate is reabsorbed |
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Tubular reabsorption
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Tubular reabsorption involves trans-epithelial transport
Active transport moves Na+ across the membrane Aldosterone promotes Na+ reabsorption (in the DCT and early collecting duct) Atrial natriuretic peptide inhibits Na+ absorption Glucose and A.A.s are reabsorbed by secondary active transport, linked to Na+ With the exception of Na+, all actively transported molecules have a transport maximum Active pumping of Na+ is responsible for the passive movement of Cl-, water, and urea In general waste products are not reabsorbed |
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Reabsorption
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Na+ is actively pumped through prox conv tubular cells back into the body (cap.s). This is Primary active transport
Glucose and amino acids move through the nephron cell walls in a co-transport mechanism (using a protein carrier molecule). This is secondary active transport. Virtually all the glucose and A.A. molecules presented to the membrane are reabsorbed. Tubular walls are permeable to water |
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Desc. Henle’s is very perm to water. Urea diffusion helps make medulla salty. Urea is trapped in the asc. DCT. End of DCT is also imperm to urea and it becomes more conc.
Urea becomes more conc. In DCT & collecting duct, because water is being reabsorbed under the influence of vasopressin. |
When vasopressin is secreted in the presence of water deficit, urea recycling concentrates in urine
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Urea Recirculation
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Urea is passively reabsorbed in proximal tubule.
In the presence of ADH, water is reabsorbed in distal and collecting tubules, concentrating urea in these parts of the nephron. The inner medullary collecting tubule is highly permeable to urea, which diffuses into the medullary interstitium. ADH increases urea permeability of medullary collecting tubule. |
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Cellular Ultrastructure and Transport Characteristics of Thin Loop of Henle
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very permeable
to H2O and doesn’t pump Na |
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Cellular Ultrastructure and Transport Characteristics of Thick Loop of Henle
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not permeable to
to H2O, pumps Na out of filtrate into tissue. H+ secreted into filtrate |
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Henle
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The descending limb is impermeable to salt diffusion
Water is drawn out and the filtrate concentrates Ascending limb pumps salt out The increased hypertonicity of the medulla is the main driving effect to pull water out of the nearby collecting ducts. |
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Cellular Ultrastructure and Transport Characteristics of Early Distal Tubules and Collecting Tubules
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not permeable
to H2O not very Permeable to urea |
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Cellular Ultrastructure and Transport Characteristics of Late Distal Tubules and Collecting Tubules
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permeablility
to H2O depends on ADH not very Permeable to urea |
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Tubular Secretion
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First step is simple diffusion from peritubular
capillaries to interstitial fluid Enter into tubular cell can be active or passive Exit from tubular cell to lumen can be active or passive Examples: potassium, hydrogen, organic acids, organic bases, NH3 |
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The most important tubular secretion processes are those for
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K+ and H+ (and some organic ions)
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Early Distal Tubule
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Functionally similar to thick ascending loop
Not permeable to water (called diluting segment) Active reabsorption of Na+, Cl-, K+, Mg++ Contains macula densa |
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The Vasa Recta Preserve Hyperosmolarity of Renal Medulla
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The vasa recta
serve as countercurrent exchangers Vasa recta blood flow is low (only 1-2 % of total renal blood flow) |
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Factors That Contribute to Buildup of Solute in Renal Medulla - Countercurrent Multiplier
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Active transport of Na+, Cl-, K+ and other ions from thick
ascending loop of Henle into medullary interstitium Active transport of ions from medullary collecting ducts into interstitium Passive diffusion of urea from medullary collecting ducts into interstitium Diffusion of only small amounts of water into medullary interstitium Urea is one of the players that keeps the counter current mech running |
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Net Effects of Countercurrent Multiplier
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1. More solute than water is added to the renal medulla
(i.e., solutes are “trapped” in the renal medulla). 2. Fluid in the ascending loop is diluted. 3. Most of the water reabsorption occurs in the cortex (i.e., in the proximal tubule and in the distal convoluted tubule) rather than in the medulla. 4. Horizontal gradient of solute concentration established by the active pumping of NaCl is “multiplied” by countercurrent flow of fluid. |
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Summary of Water Reabsorption and Osmolarity in Different Parts of the Tubule
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Proximal Tubule: 65 % reabsorption, isosmotic
Desc. loop: 15 % reabsorption, osmolarity increases Asc. loop: 0 % reabsorption, osmolarity decreases Early distal: 0 % reabsorption, osmolarity decreases Late distal and coll. tubules: ADH dependent water reabsorption and tubular osmolarity |
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Some substances have a maximum rate of tubular transport
due to saturation of carriers, limited ATP, etc. |
Transport Maximum: Once the transport maximum is
reached for all nephrons, further increases in tubular load are not reabsorbed and are excreted. Threshold is the tubular load at which transport maximum is exceeded in some nephrons. This is not exactly the same as the transport maximum of the whole kidney because some nephrons have lower transport max’s than others. Examples: glucose, amino acids, phosphate, sulfate |
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The figure below shows the concentrations of inulin at
different points along the tubule, expressed as the tubular fluid/plasma (TF/Pinulin) concentration of inulin. If inulin is not reabsorbed by the tubule, what is the percentage of the filtered water that has been reabsorbed up to that point. remains at each point? What percentage of the filtered water has been reabsorbed up to that point? |
Inulin is not reabsorbed and not secreted
Know how to calculate GFR |
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Clearance is a general concept that describes the
rate at which substances are removed (cleared) from the plasma. |
Renal clearance of a substance is the volume of
plasma completely cleared of a substance per min by the kidneys. |
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How fast can these cells pump molecules out?
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Carrier mediated transport (like Glu and A.A.s) has a maximum – when all the carriers are full. Transport Max for Glu is 375mg/min.
Fasting blood Glu = about 100mg/dl or 1mg/ml. GFR = about 125 ml/ min. Glu is filtered about 125 mg/min. Carriers are saturated at 375 mg/min Glucose – for example – arrears in the urine when more Glu passes through the tubule than the cells can pump. Glu begins to appear in the urine when plasma conc.s are 180-200ml/dl. (some nephrons have a lower threshold than others.) |
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Calculate the GFR from the following data:
Pinulin = 1.0 mg / 100ml Uinulin = 125 mg/100 ml Urine flow rate = 1.0 ml/min |
gfr=C.inulin=Uinulin x V divided by Pinulin
gfr=125x1.0 divided by 1.0 gfr =125ml/min |
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A uninephrectomized patient with uncontrolled diabetes has a
GFR of 90 ml/min, a plasma glucose of 200 mg/dl (2mg/ml), and a transport max (Tm) shown in the figure. What is the glucose excretion for this patient? |
30 mg/min
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T max
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Glucose 320 mg/min
Urates 15 mg/min Plasma proteins 30 mg/min Vit. C 1.77 mg/min Hgb 1 mg/min |
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Clearances of Different Substances
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Substance Clearance (ml/min
inulin 125 PAH 600 glucose 0 sodium 0.9 urea 70 Clearance of inulin (Cin) = GFR Clearance creatinine (Ccreat) ~ 140 (used to estimate GFR) Clearance of PAH (Cpah) ~ effective renal plasma flow |
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Clearance Technique
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Renal clearance of a substance is the volume of
plasma completely cleared of a substance per min. |
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Sodium Chloride and Potassium Transport in Thick Ascending Loop of Henle
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In the thick segment, Na+ and K+ together with 2 Cl- enter the tubular cells. Na+ is then pumped out into the interstitial space (and Cl- follows passively). The K+ can diffuse back into the filtrate. Loop diuretics block Na+ from entering the cells in the first place
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Regulation of Tubular Reabsorption
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Glomerulotubular Balance
Peritubular Physical Forces Hormones - aldosterone - angiotensin II - antidiuretic hormone (ADH) - natriuretic hormones (ANF) - parathyroid hormone Sympathetic Nervous System Arterial Pressure (pressure natriuresis) Osmotic factors |
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Aldosterone Actions on Late Distal, Cortical and Medullary Collecting Tubules
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Increases Na+ reabsorption
Increases K+ secretion Increases H+ secretion |
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Abnormal Aldosterone Production
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Excess aldosterone - Conn’s syndrome
Na+ retention, hypokalemia, alkalosis, hypertension Aldosterone deficiency - Addison’s disease Na+ wasting, hyperkalemia, hypotension |
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Control of Aldosterone Secretion
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Factors that increase aldosterone secretion
Angiotensin II Increased K+ adrenocorticotrophic hormone (ACTH) (permissive role ) Factors that decrease aldosterone secretion Atrial natriuretic factor (ANF) Increased Na+ concentration (osmolality) |
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Angiotensin II Increases Na+ and Water Reabsorption
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Stimulates aldosterone
Directly increases Na+ reabsorption (proximal, loop, distal, collecting tubules) Constricts efferent arterioles - decreases peritubular capillary hydrostatic pressure increases filtration fraction, which increases peritubular colloid osmotic pressure) |
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Angiotensin II Blockade Decreases Na+ Reabsorption and Blood Pressure
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ACE inhibitors (captopril, benazipril, ramipril)
Ang II antagonists (losartan, candesartin, irbesartan) decrease aldosterone directly inhibit Na+ reabsorption decrease efferent arteriolar resistance leads to Natriuresis and Diuresis + Blood Pressure |
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Antidiuretic Hormone (ADH)
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Secreted by posterior pituitary
Increases H2O permeability and reabsorption in distal and collecting tubules Allows differential control of H2O and solute excretion Important controller of extracellular fluid osmolarity |
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Stimuli for ADH Secretion
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Increased osmolarity
Increased osmolarity Decreased blood pressure (arterial baroreceptors) Other stimuli : - input from cerebral cortex (e.g. fear) - angiotensin II ? - nausea - nicotine - morphine |
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Factors that Decrease ADH Secretion
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Decreased osmolarity
Increased blood volume (cardiopulmonary reflexes) Increased blood pressure (arterial baroreceptors) Other factors: - alcohol - clonidine (α-2 adrenergic agonist) - haloperidol (antipsychotic, tics,Tourette’s) - caffeine |
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Stimuli for Thirst
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Increased osmolarity
Decreased blood volume (cardiopulmonary reflexes) Decreased blood pressure (arterial baroreceptors) Increased angiotensin II Other stimuli: - dryness of mouth |
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Factors that Decrease Thirst
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Decreased osmolarity
Increased blood volume (cardiopulmonary reflexes) Increased blood pressure (arterial baroreceptors) Decreased angiotensin II Other stimuli: -Gastric distention |
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Abnormalities of ADH
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Inappropriate ADH syndrome (excess ADH)
- decreased plasma osmolarity, hyponatremia “Central” Diabetes insipidus (insufficient ADH) - increased plasma osmolarity, hypernatremia, excess thirst |
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Disorders of Urine Concentrating Ability
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Failure to produce ADH: “Central” diabetes insipidus
Failure to respond to ADH: “nephrogenic” diabetes insipidus - impaired loop NaCl reabs. (loop diuretics) - drug induced renal damage: lithium, analgesics - malnutrition (decreased urea concentration)- kidney disease: pyelonephritis, hydronephrosis, chronic renal failure |
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Atrial Natriuretic Peptide Increases Na+ Excretion
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Secreted by cardiac atria in response to stretch
(increased blood volume) directly inhibits Na+ reabsorption inhibits renin release and aldosterone formation increases GFR helps to minimize blood volume expansion |
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Parathyroid Hormone Increases Renal Ca++ Reabsorption
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Released by parathyroids in response to
decreased extracellular Ca++ Increases Ca++ reabsorption by kidneys Increases Ca++ reabsorption by gut Decreases phosphate reabsorption Helps to increase extracellular Ca++ |
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Sympathetic Nervous System Increases Na+ Reabsorption
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Directly stimulates Na+ reabsorption
Stimulates renin release Decreases GFR and renal blood flow |
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Increased Arterial Pressure Decreases Na+ Reabsorption (Pressure Natriuresis)
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Increased peritubular capillary hydrostatic pressure
Decreased renin and aldosterone Increased release of intrarenal natriuretic factors - prostaglandins - EDRF |
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Osmotic Effects on Reabsorption
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Water is reabsorbed by osmosis
Decreasing the amount of solutes reabsorbed in the tubules decreases water reabsorption i.e. diabetes mellitus: unreabsorbed glucose in tubules causes diuresis and water loss i.e. osmotic diuretics (mannitol) |
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Abnormal Tubular Function: Increased Reabsorption
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Conn’s Syndrome: primary aldosterone excess
Renin secreting tumor: excess Ang II formation Inappropriate ADH syndrome: excess ADH |
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Abnormal Tubular Function: Decreased Reabsorption
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Diabetes Insipidus: decreased water reabsorption,
hypernatremia, increased thirst - nephrogenic - lack of ADH Addison’s disease: decreased Na+ reabsorption and decreased K+ secretion; lack of aldosterone |
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Abnormal Tubular Function: Decreased Reabsorption
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Fanconi syndrome: generalized decrease in reabsorption
often in proximal tubules; causes: genetic, heavy metal damage, drugs (tetracyclines), multiple myeloma, tubular necrosis (ischemia) Renal tubular acidosis: decreased H+ secretion, acidosis causes: genetic, renal injury, etc |
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Assessing Kidney Function
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Albumin excretion (microalbuminuria)
Plasma concentration of waste products (e.g. BUN, creatinine) Urine specific gravity, urine concentrating ability Imaging methods (e.g. MRI, PET, arteriograms, iv pyelography, ultrasound etc) Isotope renal scans Biopsy Clearance methods (e.g. 24-hr creatinine clearance) etc |
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Concentration and Dilution of the Urine
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Primarily controlled by ADH
Maximal urine concentration = 1200 - 1400 mOsm / L (specific gravity ~ 1.030) Minimal urine concentration = 50 - 70 mOsm / L (specific gravity ~ 1.003) |
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Water diuresis in a human after ingestion of 1 liter of water
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Even though water excretion rates change, solute excretion rates remain fairly constant
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Formation of a Dilute Urine
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Continue electrolyte reabsorption
Decrease water reabsorption Mechanism: 1. decreased ADH release 2. reduced water permeability in distal and collecting tubules |
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Formation of a Concentrated Urine
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Continue electrolyte reabsorption
Increase water reabsorption Mechanism: Increased ADH release which increases water permeability in distal and collecting tubules High osmolarity of renal medulla Countercurrent flow of tubular fluid |
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Formation of a Concentrated Urine when Antidiuretic Hormone (ADH) Levels are High
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Cells of the DCT and collecting duct reabsorb water
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Obligatory Urine Volume
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The minimum urine volume in which the excreted
solute can be dissolved and excreted. Example: If the max. urine osmolarity is 1200 mOsm/L, and 600 mOsm of solute must be excreted each day to maintain electrolyte balance, and excrete metabolic waste toxins,the obligatory urine volume is: 600/1200=0.5liter per day |
