Urinary System
Chapter 25
Urinary System Organs
• 2 Kidneys forms urine
• 2 Ureters transport urine
• Urinary bladder stores urine
• Urethra transports urine
http://findmeacure.com/2008/03/27/hematuriablood-in-the-urine/
Functions
• Primary
– Filters and excretes toxins, wastes, and ions
– Regulates blood volume, pressure, & composition
– Maintain balance in blood (H20, salt, acids &
bases)
• Supporting
– Gluconeogenesis w/ fasting
– Renin and EPO production
– Vitamin D activation
Kidney Anatomy (external)
• Paired retroperitoneal organs
– Right lower b/c liver
– Renal ptosis: kidney falls w/
emaciation  kinks ureters
• Hydronephrosis w/ resulting urine
backup
• Adrenal glands on top
• Renal hilum for vessel entry
http://www.arizonatransplant.com/image
s/kidney_large_1.JPG
Kidney Anatomy (internal)
• Renal capsule
• Renal cortex
• Renal medulla
– Renal (medullary) pyramids
w/ papilla
– Renal columns
• Renal pelvis
– Walls are smooth muscle
peristalsis
– Major and minor calyces
– Pyelitis when inflamed
• Pyelonephritis all inflamed
http://tejatechblog.blogspot.com/2010/06/internal-strutureof-kidney.html
Blood and Nerve Supply
• ¼ total CO
– 90% of supply enters cortex
• Renal plexus off of celiac plexus (SNS)
Nephron
• Forms urine from filtrate
• Renal corpuscle
– Glomerulus is a fenestrated capillaries
– Glomerular (Bowman’s) capsule surrounds
• Outer sim. squ. & inner podocyte
• Renal tubules
– PCT: sim. cub. w/ microvilli & mitochondria (cortex)
• Increase SA for absorbing H20 & solutes and secretion
– Loop of Henle: sim. cub.  sim. squ.  sim. cub/col
• Cortical vs juxtamedullary nephrons
http://kvhs.nbed.nb.ca/gallant/b
iology/nephron_structure.html
– DCT: see PCT, but no microvilli (cortex)
• Collecting ducts: sim. cub. (medullary pyramids)
– Intercalated cells: abundant microvill and maintain acid/base balance
– Principal cells: sparse microvilli and maintain H2O and Na+ balance
Nephron Blood Supply
• Glomerulus
– Afferent artery in from cortical radiate
– High BP (wider too) force solute & fluid out
– Produces filtrate
• Peritubular capillaries
– Efferent artery out
– Porous & low pressure to reabsorb filtrate (99% to
venules)
– Modified as vasa recta in juxtamedullary nephrons
Juxtaglomerular (JG) Apparatus
• Regulate BP and rate of filtrate
formation
• Specialized cells
– Juxtaglomerular (JG) cells in
afferent arteriole
• Smooth muscle w/ renin secreting
granules
• Mechanoreceptors for BP
– Macula densa in renal tubule
• Columnar cells
• Chemoreceptors for changing
[NaCl] in filtrate
http://pclab.cataegu.ac.kr/physiology/Kidney.htm
Filtration Membrane
• B/w blood and intercapsular space
• Layers
– Fenestrated epi. of glomerulus
• All, but blood cells pass
– Basement membrane (b/w epi and podocytes)
• All, but smallest proteins
• (-) electrical charge assists repulsion of (-) proteins
– Podocyte
• Filtration slits b/w feet w/additional slits prevent
macromolecule escape
Kidney Physiology (overview)
• Steps
– Cell and protein free blood into tubules/collecting
duct (1)
– Vasa recta reclaims needs and excretes rest
• All glucose, AA’s, salt, and 99% H2O (2)
– Selective addition of other molecules (3)
• Terminology
– Filtrate is everything in blood, but protein
– Urine is metabolic waste & excess substances
Glomerular Filtration (1)
• More efficient than other capillaries
– High permeability and SA of glomerulus
– Glomerular BP higher
– Higher net filtration pressure (NFP)
• H2O, glucose, AA’s, & nitrogenous waste diffuse
– Similar composition of filtrate & blood
• Large proteins prevented
– Maintain colloid pressure
– Prevent all H2O loss from blood
– Proteins in blood = imbalance
Net Filtration Pressure (1)
• Review chpt 19
– Hydrostatic pressure, fluid force on wall
• Filters fluids from cells and proteins
– Colloid osmotic pressure
• Nondiffusible molecules encourage osmosis
• Determines filtrate formation (glomerulus)
– Glomerular hydrostatic pressure pushes H2O out into
intercapsular space
– Colloid osmotic pressure of glomerular blood and
capsular hydrostatic pressure opposes
– NFP = HPg – (OPg + HPc)
Glomerular Filtration Rate (GFR) (1)
• Volume of filtrate made/min (~ 120 -125
ml/min)
• Regulation
– SA for filtration
– Filtration membrane permeability
– NFP
• Directly proportional to NFP
Intrinsic Regulation of GFR (1)
• Myogenic mechanism (JG cells monitor)
– Up systemic BP  vasoconstrict aff. art.  down flow
to glomerulus
• Decreased GFR protects glomerulus
– Down systemic BP reverses
• Tubuloglomerular feedback mechanism (macula
densa monitor)
– GFR up = insufficent reabsorption = high NaCl 
vasoconstrict aff. art. = down flow to glomerulus
• NFP and GFR down to allow time for filtration
– Low NaCl reverses
– Adaptable except low BP (< 80 mm Hg) = stops
Extrinsic Regulation of GFR (1)
• SNS maintain systemic BP
– NE w/ stress vasoconstrict aff. art.  down filtrate
formation
– Stimulates macula densa and JG cells
• Renin – angiotensin mechanism restores blood
volume and BP
– Renin converts angiotensinogen to angiotensin I
• Renin w/ down stretch, activation by macula densa, and Epi
receptor stimulation
– Angiotensin I to angiotensin II
• MAP up (vasoconstriction)
• Increase Na+ reabsorbed by PCT
• Adrenal cortex release aldosterone
Tubular Reabsorption (2)
• All glucose and AA’s
• H2O and ions dependent on
hormones
• Can be active or passive
– Transcellular route though
renal tubule cells
• Lumen and basement membrane
 peritubular capillaries
– Paracellular route between
renal tubule cells
• Tight junctions hinder, but in PCT
(Ca2+, Mg2+, K+, & Na+)
Na+ Reabsorption(2)
• Primary cation in filtrate moved actively
– 1° active transport:
• Na+-K+ ATPase pumps Na+ into interstitial fluid
• Low HP and high OP (undiffusible proteins) into
capillaries
– 2° active transport
• From (-) electrochemical gradient primary set up
– Na+ low inside and K+ rapidly leak out
– Na+ passively into cells (facilitated diffusion)
• Cotransport of glucose, AA’s, lactic acid ,and vitamins
More Reabsorption(2)
• Passive tubular transport from 1° and 2° active
transport
– Aquaporins
• Responsible for obligatory H2O reabsorption in PCT
• Absent in collecting ducts w/o ADH
– Up [solute] in filtrate  solutes diffuse out
• Lipid soluble toxins and drugs also
– (-) electrochemical gradient  anions diffuse out
• Transport maximum (Tm) reflects number of carriers
present
– Relative to need for molecule
– At saturation excess molecules excreted
• Diabetes mellitus has increase [glucose] in urine
Renal Tubular Activity (2)
• PCT (previously) most active
• Loop of Henle
– Descending H2O in, but no ascend [aquaporins]
– Solutes opposite
– Role in dilute vs concentrated urine
• DCT
– Depends on body needs
• ADH adds aquaporins = H2O reabsorption up
• Aldosterone (renin-angiotensin) up Na+ reabsorption
– H2O follows = BP increase
• ANP encourages Na + loss
– W/ high atrial pressure to drop blood volume and pressure
Diuretics (2)
• Chemicals enhancing urine output
– Substances nor reabsorbed
– Substances exceeding renal tubules ability to
reabsorb
– Substances inhibiting Na+ reabsorption
• Alcohol inhibits ADH (H2O reabsorption)
• Caffeine, drugs, and other Na+
reabsorption inhibitors
• Stop obligatory H2O reabsorption
Tubular Secretion (3)
• Reabsorption in reverse
– PCT mainly, but cortical collecting ducts too
• Functions
– Eliminate drug bound proteins (not filtered)
– Eliminate urea and uric acid (protein metabolism)
– Eliminate excess K+ ions
– Control blood pH
• Up acidity = excess H+ in urine and HCO3- reabsorbed
• Down acidity = HCO3- in urine and Cl- reabsorbed
Ureters
• Two tubes containing a tri-layered wall
– Transitional epi. mucosa (kidney pelvis and bladder too)
– Inner longitudinal & outer circular smooth muscle
• 3rd external longitudinal layer in lower 1/3
– Fibrous CT adventitia
• Urine transport through peristalsis
– Stretch signal more than neural
• Imbalances
– Renal calculi (kidney stones) from Ca2+, Mg2+, or uric acid
salts precipitating
• Bacterial infections, urine retention, high ion levels, and alkaline
pH predispose
• Cranberry juice acidifies and H2O dilutes
Urinary Bladder
• Ureteral and urethral orifices form trigone
– Common site of infections
• Similar tri-layer wall as ureters
– Middle layer resemble lower 1/3 ureter = detrusor
muscle
– Walls w/ rugae for distension
Urethra
• Trans.  pseudostrat. colum.  strat. sqam.
• Internal urethral sphincter @ junction w/ bladder
– Contraction opens
• External urethral sphincter @ urogenital diphragm
– Levator ani assists
• External urethral orifice
• Males w/ 3 regions
– Prostatic, membranous, and spongy
• Imbalances
– Dysuria (painful urination)
• Indicators: up urgency, frequency, and/or presence of blood
– UTI’s from bacterial infections
• Females predisposed b/c location, intercourse, wiping
• Can cause urethritis, cystitis, pyelitis , inflammation of urethra,
bladder, or kidney
Urine Characteristics
• Color and turbidity
–
–
–
–
Yellow shades from urochrome, product of Hb breakdown
Higher concentration is darker yellow
Abnormal colors from foods, bile pigments, or blood
Cloudiness could indicate UTI
• Odor
– Fresh is aromatic, but standing more ammonia b/c bacterial activity
– Drugs, vegetables (asparagus & onions), & diseases can alter
• pH
– Usually ~ 6
– Down w/ acidic diet (high protein, whole wheat)
– Up w/ vegetarian diet, prolonged vomiting, and infection
• Specific gravity, ratio of urine to dH2O
– Higher than 1.0 b/c H2O + solutes
– [solutes] determines, 1.001 – 1.035 is normal
Chemical Composition of Urine
• 95% water
• 5% solutes
– Nitrogenous wastes
• Urea, uric acid, and creatinine (AA, nucleic acid, & CP
breakdown respectively)
– Na+, K+, Ca2+, Mg2+, HCO3- also
• Abnormal amounts, protein, or WBC presence
indicates disease/imbalance
Micturition (Urination)
• Voiding of bladder
• Distension of bladder walls initiates spinal reflex
– Contraction of external urethral sphincter
– Inhibit detrusor muscle and internal sphincter
(temporarily)
• Reflexive control till ~ 2 or 3 years of age (pons)
• Incontinence when can’t control
– Laughing and coughing up abdominal pressure
– Pregnancy stretches muscles
• Urinary retention when can’t go
– Common after anesthesia or w/ prostate enlargement