1. Chapter 24 Urinary System1 1

2. Organs of the Urinary System
Kidneys (2)
Ureters (2)
Urinary bladder (1)
Urethra (1)

3. Functions of the Kidney
Filters blood plasma-removes waste products, toxins, H+, drugs, hormones, water, urea
Produces urine
Regulate blood volume and pressure
Secretes erythropoietin stimulates production of RBC cells
Regulates the osmolarity of the body fluids
Collaborate with lungs to regulate/buffer PCO2 and acid-base balance (pH)
Regulates plasma ion concentrations
Sodium, potassium, and chloride ions controlling urine loss
Calcium ion levels through synthesis of calcitriol-Vitamin D helps to regulate calcium homeostasis
Kidney cells can engage in Gluconeogenesis from amino acids in extreme starvation 3

4. KIDNEYS 3 layers of CT tissue:
Renal fascia: dense, fibrous outer layer binds kidney to abdominal wall
Perirenal fat capsule: thick layer of adipose tissue cushions/holds in place
Renal/fibrous capsule: layer of collagen fibers encloses the kidney. On top of kidney

5. Anatomy of the Kidney Cortex: outer layer of the kidney
Medulla: middle layer composed pyramids and renal columns.
Pyramids: collecting ducts/ loops of Henle, lower portion of the nephrons.
Renal columns –extension of cortex
Renal sinus: internal cavity within kidney; stabilizes positions of ureter, renal blood vessels, and nerves
The papilla of each pyramid projects into the calyx.
Calyces collect the urine released from the papillae and allow it to drain into an enlarged collection
minor calyx – drains papilla
major calyces – drains minor calyx
renal pelvis -connected to ureter, which drains kidney
Lobe of the kidney = 1 pyramid and overlying cortex; produces urine
Hilum - entry for renal artery and renal nerves; exit for renal vein and ureter

7. Blood supply
Kidneys are highly vascular necessary for its function; receives 20%–25% of total cardiac output
Path of blood through the kidney:
renal artery  segmental arteries  interlobar arteries  arcuate arteries  cortical radiate arteries (interlobular artery)  afferent arterioles  glomerular capillaries  efferent arterioles  peritubular capillaries and vasa recta  venules  cortical radiate veins (interlobular vein)  arcuate veins  interlobar veins  renal vein  inferior vena cava
(Interlobular veins)
(Interlobular artery)

9. Blood Supply to the Kidneys
Figure 24.8

12. The Nephron Functional unit of the kidney Renal corpuscle
Glomerular capsule (Bowman’s capsule)
Capillary network (glomerulus)
Renal tubule
Begins at renal corpuscle
Located in cortex
Proximal convoluted tubule (PCT)
Loop of Henle
Extends partially into medulla
Distal convoluted tubule (DCT)
The nephron receives blood from the afferent arteriole.
The afferent arteriole supplies the glomerulus
From the glomerulus blood flows into the efferent arteriole.
The efferent arteriole flows into more capillaries, the peritubular capillaries, and, in juxtamedullary nephrons, the vasa recta.
Peritubular capillaries and vasa recta lead to the venous drainage of the kidney.

13. Types of Nephrons Cortical nephrons 85% of all nephrons
short nephron loops
efferent arterioles branch into peritubular capillaries around PCT and DCT
Juxtamedullary nephrons
15% of all nephrons
very long nephron loops, maintain salinity gradient in the medulla and helps conserve water
efferent arterioles branch into vasa recta around long nephron loop

14. Renal Corpuscle Bowman’s capsule and glomerulus.
Filtration unit of the nephron - produces protein-free solution (filtrate) similar to blood plasma
HBP forces water and dissolved solutes out of glomerular capillaries into Bowman’s capsular space
The outer (parietal) layer of Bowman's capsule consists of simple squamous epithelial cells with tight junctions; serves to contain the filtrate in the capsular space.
The visceral epithelium of the Bowman's capsule consists of large cells called podocytes with complex processes or “feet” (pedicels) that wrap around specialized dense layer of glomerular capillaries to produce openings called filtration slits.
The glomerulus - condensed mass of fenestrated capillaries allows substances to escape by filtration.

15. Filtration Membrane
3 layers lie between blood and the interior wall of glomerulus capsule.
Fenestrated capillary endothelium -prevents release of blood cells
Basement membrane
Visceral membrane on glomerulus-podocytes/pedicels/ /filtration slits
1000x more permeable to water and solutes than other capillaries.
Kidney infections / trauma can damage filtration membrane allowing proteins and blood cells to escape into filtrate and be released into the urine.

16. Nephron Tubules Tubular Cells form the tubular portion of the nephron
Absorb organic nutrients, ions, water, and plasma proteins FROM the tubular fluid
RELEASES them into peritubular fluid
(INTERSTITIAL FLUID around renal tubule
Three (3) Functions of the Renal Tubule
Reabsorb useful organic nutrients that enter filtrate and RETURN them to blood
Reabsorb more than 90% of water in filtrate RETURNS to blood
Secrete waste products into the filtrate that failed to enter renal corpuscle through filtration at glomerulus

18. Collecting duct
The distal convoluted tubule (DCT) opens into the collecting system
Multiple nephrons drain into a nearby collecting duct; NOT PART OF THE NEPHRON
Several collecting ducts converge into a larger papillary duct that empties into a minor calyx carrying tubular fluid to renal pelvis.
Determines final osmotic concentration and volume of urine
Reabsorbs Na+, bicarbonate, and urea
Secretes hydrogen or bicarbonate ions to control body fluid pH
Aldosterone controls Na+ pumps and channels in collecting duct reducing loss of Na+ in urine
ADH controls permeability to water (aquaporins)

19. Ureters
From the collecting ducts urine passes through the papillary ducts, the minor calyces, the major calyces, and the renal pelvis.
The ureters are connected to the renal pelvis and carry urine to the urinary bladder for storage.
Urine travels by peristalsis.
Ureteral openings are slit-like rather than rounded to prevent backflow of urine. When bladder contracts no valves/sphincters but expansion of the bladder puts pressure on ureters preventing backflow of urine and possible infection.
Outer layer made of fibrous connective tissue.
Ureters have TWO layers of smooth muscle (muscularis) in their wall: a longitudinal layer (outermost) and a circular layer (innermost).
The lining of the ureters is made of transitional epithelium which allows them to stretch and reduce back pressure on the kidney.
Lumen very narrow easily obscured or injured by kidney stones
Micturition (urination) occurs when sphincters of the urethra open to allow urine to flow out of the body.

20. Urinary Bladder
Hollow muscular and elastic organ stores urine.in lower pelvic cavity.
3 layers: the mucosa, the detrusor muscle, the adventitia
The mucosa comprised of transitional epithelium supported by a lamina propria. Transitional epithelium can be stretched
Epithelial cells secrete mucus for protection from acidity of urine.
Rugae allow bladder to expand and return to its original shape.
Detrusor muscle - two layers of longitudinal smooth muscle (outer and inner layers), and a middle circular layer. Can spasm during infection
The internal urethral sphincter (involuntary) is part of the detrusor muscle.
The external urethral sphincter (voluntary) is part of the urogenital diaphragm
The fibrous adventitia covers the bladder
Opening of the two ureters and urethra mark a smooth surfaced triangular area called the TRIGONE on the bladder floor. Common site of bladder infections.

21. Urinary Bladder

22. Urethra Tubular organ that allows drainage of the urinary bladder.
Near the bladder urethra lined with transitional epithelium and near the external urethral orifice it is stratified squamous.
In males the urethra is subdivided into 3 regions: prostatic, membranous, and spongy regions.
In females short tubule. Its external orifice is located within vulva.

23. Micturition and Incontinence
Urine pressure stimulates receptors in the bladder wall: triggers a parasympathetic reflex causing detrusor muscle contractions and relaxation of internal urethral sphincter initiating micturition/urination
The need to urinate cannot be repressed but the delivery of urine can be delayed by the voluntary external urethral sphincter.
If the need to urinate arises and is inconvenient, stretch receptors will fatigue and stop firing. Continued tension in the bladder will resume firing with increased frequency.
When conditions are appropriate, parasympathetic stimuli relax the external sphincter. 
INCONTINENCE = Absence of control of urination:
Normal in children less than 3 years old
Newborns void frequently as the bladder is small
kidneys cannot concentrate urine until 2 months of age.
Children- Voluntary control of the urinary sphincters depends on nervous system development
complete bladder control during the night does not usually occur before 4 years of age.
Children may be trained to develop control of the external urethral sphincter.
Adults disorders caused by paralysis, stress, traumatic injury, caffeine consumption, prostate issues, aging.

24. Urinary System Disorders
UrinaryTract Infection (UTI)
cystitis – infection of the urinary bladder
pyelitis – infection of the renal pelvis from blood borne agents such as bacteria.
pyelonephritis – infection that reaches the cortex and the nephrons. ie: kidney infection
Escherichia coli (e-coli) bacteria often associated with infection
Kidney stones form in renal pelvis- hardened mineral deposits
Glucosuria excretion of glucose in urine
Retention - failure to eliminate urine normally; may require insertion of catheter to allow urine to flow out. Potential cause-prostate; anesthetic
Renal insufficiency –75% of nephrons are lost
urine output (GFR) of 30 mL/hr is insufficient (normal mL/hr) to maintain homeostasis
Causes:hypertension, diabetes, chronic kidney infections, trauma, CAN SURVIVE WITH ONLY 1/3 OF ONE KIDNEY!!
Approximately1/3 of people with diabetes are susceptible to chronic kidney disease.
Uremia- 90% loss of kidney function
Nephrons can regenerate restoring kidney function following short-term injury
23-24

25. Nitrogen Waste Removal
Nitrogenous wastes result of protein metabolism Proteins amino acids NH2 removed  forms ammonia  liver urea
UREA formation accounts for 50% of waste products
Waste dissolves in blood; lost in urine; produce some H2O loss
Uric acid- product of nucleic acid catabolism (DNA purines =adenine/guanine); “gout”
Measurement of Waste products
Measured using BLOOD UREA NITROGEN (BUN)
normal concentration of blood urea is 10 – 20 mg/dl
azotemia – elevated BUN indicates renal INSUFFICIENCY
Could also be the result of dehydration or shock
severe toxicity of nitrogenous waste –indicates RENAL FAILURE
Requires hemodialysis or organ transplant
CREATININE product of creatine phosphate catabolism in muscle cells. Little-to-no tubular reabsorption of creatinine; eliminated in urine. Kidney function inadequate, blood levels rise (10mg/dl); used to determine inadequate kidney function Normal = 0.6 to 1.2 mg/dL
Renal clearance test: polysaccharide – inulin is injected in blood  its excretion in urine is tracked. Inulin not metabolized by the body, nor reabsorbed.

26. Gout

27. Hemodialysis Peritoneal Dialysis
Treatment for loss of kidney function
Hemodialysis is the artificial clearing of blood wastes. Blood pumped from radial artery to a dialysis fluid. As blood flows thru semipermeable cellophane tube excess fluid, urea, K+ and other waste products are removed via diffusion. Glucose, electrolytes and drugs can be added to dialysate.
In peritoneal dialysis wastes and water are removed from the blood using the peritoneal membrane of the peritoneum. Not as efficient; increased risk of infection
Good Animation:

28. Urine Formation Three processes of urine formation:
Goal of urine production is to maintain homeostasis by regulating volume and composition of blood including excretion of metabolic waste products
Three processes of urine formation:
Glomerular Filtration
Tubular reabsorption
Tubular secretion

29. Overview of Processes of Urine Formation
Figure 24.10

30. Mechanism of Urine Formation Glomerular Filtration
Each day the kidneys process about 200 quarts of blood to sift out approximately 2 quarts of waste products and extra water. Filtration produces a protein -free solution known as filtrate combination of water and solutes filtered from blood plasma.
Filtrate moving through tubules is tubular fluid.
Filtration averages 125 ml/min for the two kidneys. This amounts to about 180 liters/d males; 150 L/d females.
Urination 1% of the filtrate; 99% reabsorbed into the blood.
Small molecules (water, electrolytes, urea, uric acid, glucose, amino acids, bicarbonate, toxins, drugs, H+, creatinine) pass from the blood through the capillaries of the glomerulus into the capsular space of the Bowman’s capsule. Fluids and solids are forced through porous 3-layered filtration membrane by HYDROSTATIC PRESSURE.
Large protein molecules and blood cells do not move out of the blood into Bowman's capsule.

31. Filtration Pressure
Glomerular blood hydrostatic pressure (GBHP) force fluids/ solute out of the glomerulus capillaries.
Pressure is higher here than other capillaries due to large afferent arteriole inlet to capsule; smaller efferent outlet
Capsular hydrostatic pressure (CsHP)
Blood colloid osmotic pressure -pull exerted by glomerular proteins; draws water out of filtrate and back into plasma
Net filtration pressure is the average GBHP – CHP – BCOP = NFP

32. Glomerular Filtration Rate
GFR amount of filtrate kidneys produce each minute; highly regulated
Only way to adjust GFR from moment to moment is to change the glomerulus blood pressure (BHP)
RENAL AUTOREGULATION
Myogenic mechanism
Juxtaglomerular Complex (JGC)
Nervous System: SYMPATHETIC Innervation - Adjusts RATE of urine formation Changes blood flow and BP at nephron
RATE TOO HIGH - fluid is moving too fast; unable to REABSORB water and solutes or remove waste/undesirable substances- can result in dehydration.
RATE TOO LOW- fluid is moving too slow; can reabsorb waste products into blood that should be eliminated in the urine; azotemia may occur
Hormonal - RASS - Sympathetic nervous system stimulates release of enzyme RENIN to restricts loss of water and salt in urine (aldosterone formation) stimulates reabsorption; increases BP

33. GFR Regulation: Renal Autoregulation
Regulates GFR by altering diameters of the nephron efferent arterioles, afferent arterioles, and gomerular capillaries.
MYOGENIC MECHANISM
Kidney filtration is affected by systemic BP
When systemic BP is ELEVATED it restricts blood flow to afferent arterioles The Myogenic mechanism
Dilates afferent arteriole- flow will increase
Constricts efferent arterioles – slows flow blood down in glomerulus
When systemic BP DROPS it INCREASES blood flow
myogenic mechanism constricts afferent arterioles; produces more resistance decreasing glomerular blood flow

34. GFR Regulation Renal Autoregulation
Juxtaglomerular Complex (JGC)
Macula densa - specialized cells located in the DCT Increase/decrease GFR by dilating or constricting afferent arteriole
Vasoconstriction of the afferent arteriole in response to RAPIDLY FLOWING FILTRATE and/or changes in osmolarity
SLOWS the GFR - more time for filtrate processing.
Vasodilation of the afferent arteriole when the filtrate is FLOWING SLOWLY or there is low osmolarity
INCREASES the GFR, preventing reabsorption of harmful substances.
Stimulates JG cells secretion of RENIN increasing release of aldosterone.
Juxtaglomerular cells – (granular) modified smooth muscle cells primarily in the walls of the afferent arteriole; synthesize, store, and secrete the enzyme RENIN = released when 1) BP drops 2) loss of aldosterone 3) sympathetic nervous system activity.
Mesangial cells specialized smooth muscle cells inside/outside glomerulus – regulate blood flow and blood pressure; produce prostaglandins for local hormonal regulation to control blood flow

35. Mesangial produce prostaglandins to regulate blood flow locally.
JG Cells
Mesangial produce prostaglandins to regulate blood flow locally.

36. GFR Regulation Nervous/Hormonal Regulation
Changes in BP, blood volume; osmolarity of tubular fluid near macula densa
ACTIVATES hormonal regulation.
Sympathetic Nervous System activates the Renin Angiotensin Aldosterone System (RAAS) mechanism:
SNS causes release of the “ENZYME” Renin by JG cells.
Renin converts the liver plasma protein angiotensinogen to the peptide angiotensin I.
Angiotensin I converted to “HORMONE” angiotensin II by angiotensin converting enzyme – ACE produced in the LUNGS/KIDNEYS
Angiotensin II causes constriction of the EFFERENT arteriole increasing glomerular hydrostatic pressure, and increasing GFR.
Angiotensin II stimulates release of aldosterone.
Controls Na+ pumps and channels both the DCT and Collecting duct reducing loss of Na+ in urine. Na+ gain proportional to K+ loss.
Atrial natriuretic peptide (ANP) from atria in response to increased blood volume or pressure
Triggers “dilation” of AFFERENT arterioles
Triggers “constriction” of EFFERENT arterioles
Elevates glomerular pressures and INCREASES GFR

37. Renin stimulated by Sympathetic Nervous System
Renin stimulated by JG cells
Plasma protein –made in liver
(Enzyme from JG cells)
Renin stimulated by Sympathetic Nervous System
Peptide
(ACE)
Hormone – from lungs and liver
Efferent arteriole
in the heart ventricles

38. Urine Formation Three processes of urine formation
Glomerular Filtration
Tubular reabsorption
Tubular secretion

39. Tubular reabsorption
Process where solutes and water are removed from the tubular fluid and transported into the blood. It is called reabsorption (and not absorption) because these substances have already been absorbed once (intestines) and because the body is reclaiming them from a post-glomerular fluid stream that will become urine.
Reabsorption is a two-step process beginning with the active or passive extraction of substances from the tubule fluid into the renal interstitium and then the transport of these substances from the interstitium into the blood.
Transports mechanisms
Paracellular reabsorption via diffusion between cells – solvent drag
Transcellular reabsorption through the bottom of the cells
Transcellular absorption increases due to water channels called aquaporins in the plasma membrane – controlled by ADH
Two types of transport proteins channels Symports simultaneously bind Na+ and other solutes such as glucose (SGLT). Antiports pull Na+ into cell while pumping H+ out of the cell into the tubular fluid.
Some transport proteins channels require ATP (Na+K+Pump); others are passive

40. Transport maximum (Tm) is the maximum rate of absorption reached when transporters (ex: symports, antiports) are FULL
If quantity of nutrients exceed the transport capacity of the cells, the excess nutrients are NOT REABSORBED AND PASS INTO URINE.
Renal threshold is the plasma concentration at which a specific compound or ion begins to appear in urine
When blood glucose levels are very high such as in diabetes mellitus, a large amount of glucose passes into the filtrate

42. Reabsorption: Nephron PCT
PROXIMAL CONVOLUTED TUBULE: simple cuboidal epithelial cells.
65% of glomerular filtrate fluid
regulates the pH by exchanging hydrogen ions in the interstitium for bicarbonate ions in the filtrate
Almost 100% of glucose / 90% of bicarbonate and H2O,
65% Na+, K+ / 50% Cl- / 85% P
40%-60% of urea also reabsorbed.
PTH inhibits phosphate absorption when levels create risks of calcium phosphate formation leading to hard deposits
One of the most important functions of the PCT is sodium (Na+) reabsorption.
Sodium ions are ESSENTIAL FOR REABSORPTION. They creates osmotic and electrical gradient that drives absorption of water and other solutes.
Na+ / K+ ATPase pumps prevent the accumulation of Na+ in tubule epithelial cells and sends it to the renal interstitium
Reabsorption of salt and other solutes increases the osmolarity of the interstitium, and lowers the osmolarity of the tubular cells.
Water follows the solutes into interstitium by osmosis.

43. Proximal Convoluted Tubules PTH stimulation on PCT and DCT
Reabsorption
Proximal Convoluted Tubules
PTH stimulation on PCT and DCT

44. Reabsorption: Loops
The remaining filtrate contains water, urea, sodium and other electrolytes that will be reabsorbed along the remaining tubules.
Descending thin portion of LOOP OF HENLE: simple squamous Filtrate passes through environment of increasing osmolarity (high solute, sodium, concentration).
FREELY PERMEABLE TO WATER but not to Na+
H2O passes from tubule into extracellular fluid leaving salt behind
the tubular filtrate becomes more and more concentrated.
Ascending thick portion of LOOP OF HENLE: simple cuboidal cells (IMPERMEABLE TO WATER BUT PERMEABLE TO NA+).
Fluid flowing upward in ascending limb impermeable to water
Na+, K+, and Cl- moved by active transport pumps into extracellular fluid
increases osmolarity of the surrounding interstitium of renal medulla causes tubular fluid to become hypotonic (low volume of solutes) due to loss of solutes This causes fluid to be draw from tubules into interstitium concentrating the filtrate destined to become urine.

46. Higher NaCl concentration in tubule moves to a lower concentration
Water follows Na+ concentrating fluid that remain in tubule as it reaches CT
Higher the interstitium osmolarity more water leaves the descending loop
The more water that leaves the tubules, the higher the salt content or osmolarity of the “TUBULAR” FLUID
Higher NaCl concentration in tubule moves to a lower concentration

47. Loops of Henle: Countercurrent Multiplier
The ability of kidney to concentrate urine depends on salinity gradient in renal medulla. Without the concentration, large amounts of fluid would be lost in the urine leading to recurring episodes of dehydration. The countercurrent multiplier is a concentration gradient between the loops of Henle and the blood (vasa recta)
Creates 4x saltier interstitial fluid in renal medulla than the cortex
multiplier - the two loops multiply the osmotic gradient between tubular fluid and interstitial space by continually recapturing Na+ and returning it to extracellular fluid of medulla
countercurrent - fluid flowing in opposite directions
Vasa recta – capillary branching off efferent arteriole in medulla
provides blood supply to medulla BUT DOES NOT REMOVE NaCl and urea from medullary extracellular fluid
This mechanism allows vasa recta capillaries to deliver nutrients and oxygen to kidney cells and pick up waste products and CO2 without disrupting the osmolarity gradient of the medulla.
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49. Reabsorption Distal Convoluted Tubules
DCT regulates pH by absorbing bicarbonate and secreting protons (H+) into the filtrate, or by absorbing protons and secreting bicarbonate into the filtrate.
Participates in Ca2+ regulation by reabsorbing Ca2+ in response to PTH
Sodium and potassium levels are controlled by secreting K+ and absorbing Na+ out of tubular fluid
Sodium absorption by the distal tubule is mediated by aldosterone
Aldosterone controls Na+ pumps and channels reducing loss of Na+ in urine
WATER REABSORPTION in the DCT is regulated by hormones: ADH, aldosterone, Atrial natriuretic peptide (ANP)
ADH allows water to be reabsorbed from DCT and collecting duct and not lost in urine. Stimulates synthesis of aquaporins in plasma membrane of tubules. Serve as water channels allowing more release of fluid from tubules.
Overhydration causes low blood osmolarity which slows the release of ADH -- dilute urine is produced.
ADH deficiency causes the production of a large amount of dilute urine, a condition called diabetes insipidus.

53. Collecting Duct
Regulation of water and solute loss in the Collecting Duct is controlled by aldosterone and ADH.
Aldosterone increases the number of Na+/K+ pumps that allow increased sodium reabsorption and potassium secretion. Na+ is reabsorbed into the blood, K+ is secreted in urine
Stimulates thirst in hypothalamus which then triggers release of ADH
Stimulates reabsorption of water in distal portion of DCT and CD collecting system
Exposure to ADH determines final urine concentration
Final adjustments in volume and osmotic concentration of tubular fluid occurs in DCT and Collecting duct
UREA is a waste product of protein metabolism that is passively reabsorbed from the nephron contributing to interstitial fluid hypertonicity (high volume of solutes)
Overall, MORE urea passes into urine than is reabsorbed causing a net loss of urea from the body; remains concentrated in the CD
Recycling of urea: lower end of CD permeable to urea
continually cycled from CD to the nephron loop and back

54. Urine Formation Three processes of urine formation
Glomerular Filtration
Tubular reabsorption
Tubular secretion

55.
3. Tubular Secretion
Secretion is the release of substances INTO FILTRATE FROM THE BLOOD by Substances excreted in the urine.
The substances secreted into the filtrate are mainly derived from the peritubular capillaries.
Occurs concurrently with reabsorption in the proximal convoluted tubule, the distal convoluted tubule, and the collecting duct.
Purpose of Secretion:
1) Eliminate remaining toxins and drugs not already filtered
move from the peritubular capillaries directly into tubules of the nephron and pass into urine.
2) Establish electrolyte balance.
Provides balance in electrolyte concentrations (Na+ K+ Cl-)
Maintains Bicarbonate ions as buffering agents
3) Acid / base balance: Elimination and management of H+

56. Animations
Good overview of kidney and nephron (6+mins)
Good Summary (3+mins)
Good animation urine formation
Good overview of urine production animation

57. Glomerulus- produces filtrate similar to blood plasma w/o proteins
PCT reabsorbs 65% of glomerular filtrate and returns it to peritubular capillaries
Nephron loop reabsorbs another 25% of filtrate
DCT reabsorbs Na+, Cl- and water under hormonal control, especially aldosterone and ANP
The tubules extract drugs, wastes, some solutes from the blood ; secrete them into the tubular fluid
DCT completes the process of determining the chemical composition of urine
Collecting duct conserves water; releases urine

58. Love your Kidneys!