Lu Ning 卢 宁
Associate professor
Department of Physiology and
Pathophysiology
Buiding 7, Rm 219 Tel:54237452
Luning7@shmu.edu.cn
intenet classroom: ID -Ning
Medical education between
China
and
USA
‹ High
school
medicine (5-8y)
Resident
Doctor
High school
Biology (4y)
medical college (4y)
Exam
Resident
Doctor
Reunion
flower show
Shanghai plant garden
Painting Exhibition
(2010.3.10-6.6)
82 pieces works
during the 15-20th
century
saved by Italy Museum
Shanghai Museum
“陈逸飞 Art Exhibition”
Shanghai Art gallery
2010.4.10-5.9
Kidney
Urine formation and
excretion
Urinary System
Renal failure
Overview – Functions of the Kidney
Urine
formation
filtration
Selective reabsorption
secretion
Regulation of body fluid osmolality and
volumes
Regulation of electrolyte and water
Excretion of waste products
Regulation of acid- base balance
Functions of the Kidney
‹
Regulation of body fluid osmolality and volumes
maintain cell volume
normal function of the cardiovascular system
‹
Regulation of electrolyte and water
Na+ , K + ,Cl -, HCO3 -, H +, Ca + (excretion=intake)
‹
Excretion of waste products
(Urea, Uric acids, creatine)
‹
Regulation of acid- base balance
Functions of the Kidney
‹ Production
of hormones
erythropoietin: stimulate red blood cell
formation by bone marrow
eg: Anemia
renin: renin-angiotensin-addsterone system
Calcitriol : a metabolite of Vit D3
Renal failure
Urine Formation
Structure of the Kidney
一、nephron
1～ 1.2 million each
Renal
corpuscle
Renal
tuble
glomerulus
Bowman’s capsule
proximal tubule
loop of henle
distal tuble
nephron
Nervous System
Urinary System
Cortical nephron and Juxtamedullary
nephron
Cortical
location
size
A./A.E (efferent)
ratio
in diameter
A.E
function
Juxtamedullary
85％
15％
short
loog
2：1
1：1
Peritubular
capillaries
Vasa recta,
peritubular
capillaries
Filtration and
reabsorbtion of
salt
Concentration and
diluting
Nephron
Cortical nephron and Juxtamedullary
nephron
Cortical
Juxtamedullary
85％
15％
short
loog
A./A.E ratio
in diameter
2：1
1：1
A.E
Peritubular
capillaries
Vasa recta
Filtration and
reabsorbtion
Concentration
and diluting
location
size
function
球旁器
juxtaglomerular apparatus
1) The juxtaglomerular cells:
renin-producing granular
cells
2) Macula densa
3) Extraglomerular mesangial cells
(Mesangial cell)
Juxtaglomerular apparatus
juxtaglomerular apparatus
1. juxtaglomerular cell
granular cells:
modified smooth muscle cells
Produce ,store and release renin
juxtaglomerular apparatus
2. macula densa：
detecting change of
NaCl content → send a
signal to the renal
arterial system
juxtaglomerular apparatus
3. extraglomerular
mesangial cell:
phagocytic
Blood Supply (main filtration:
in cortex of nephron)
RBF:1200 ml/min, 20-25 %
of the cardiac output
94 % through the cortex;
5-6 % through the outer
medulla;
< 1 % through the inner
medulla
nephron
Capillary
Regulation of Renal Circulation
1.Autoregulation of Renal Circulation
Relatively constant of RBF and GFR,when the range
of arterial blood pressure: 80 to 180mmHg
Mechanisms of autoregulation:
1) Myogenic mechanism
2) Flow dependent mechanism
(tubuloglomerular feedback)
Regulation of Renal Circulation
1. Autoregulation
1) Myogenic mechanism:
an increased arterial
blood pressure →→
contraction of the vascular
smooth muscle →→
constriction of the blood
vessel →→ the blood
flow is maintained
relatively constant
Regulation of Renal Circulation
2) Tubuloglomerular feedback:
an increased in renal blood flow →→
change in glomerular filtration →→
change in Na+ content in the renal filtrate
→→ detected by the macula densa →→
send a signal to the renal arterial system →→
restore RBF and glomerular filtration rate
(GFR) to normal
Tubuloglomerular feedback:
2. Neural and Hormonal Regulation
1) Neural Regulation
strong activation of the renal
sympathetic nerves →→ constrict the renal
arterioles →→ ↓renal blood flow and GRF
2. Neural and Hormonal Regulation
2) Hormonal Regulation
9 Norepinephrine,
Epinephrine, and
Endothelin
constrict renal blood vessel and ↓GFR
9 Angiotensin
II
constricts efferent arterioles
9 Nitric
Oxide
↓renal vascular resistance and ↑GFR
9 Prostaglandins
and Bradykinin
tend to increase GRF
Glomerular Filtration
Glomerular Filtration Rate
‹ Definition:
When blood passes through glomerular
capillaries, part of blood plasma free of
proteins is filtered into Bowman’s space.
the volume of fluid filtered from the
glomeruli into Bowman’s space per unit
time is termed the GFR.
Glomerular Filtration
substance
Na+
K+
ClUrea
NH3
Glucose
protein
ultrafil
Excreted Excreted／
plasma
tred
plasma
(g/L)
(g/L)
(g/L)
1.1
3.5
3.3
3.3
7.5
1.5
0.2
0.2
1.6
6.0
3.7
3.7
60.0
20.0
0.3
0.3
400.0
0.4
0.00
0.001
0
0
1.0
1.0
0
0
0.3
70～90
Glomerular Filtration
Glomerular filtration barrier
z
Structure of the filtration membrane:2-4nm
1) Capillary endothelium:
fenestration: 70~90 nm
2) Basement membrane:
meshwork of collagen and proteoglycan fibrillae: 2~8 nm
3) Epithelial cells of the renal capsule: nephrin
slit pore: 4~11 nm
Glomerular filtration barrier
the filtration membrane
Glomerular filtration barrier
z
influence of size and electrical
charge of dextran on its
filterability
Glycoproteins
z Immunolgical
damage and
inflammation
z
dextran
Cationnic molecules are more readily
filted than are anionic molecules.
The reduced filtration of anionic
molecules is explained by the presence
of negively charged glycoprotein on the
surface of all component of the
glomerular filtration barrier.
Alport syndrom
‹ Nephrin
is a transmembrane protein
(slit diaphragm)
Alport syndrom is characterrized by hematuria
and progressive glumerulonephritis and
account for 1%-2% of causes of end-stage
failure.
Nephrotic syndrome
An increase in the permeability of the
glomerular capilaries to proteins
proteinuria
edema, hypoalbuminemia
Glomerular Filtration
1) The Glomerular filtration rate (GFR)
Defined as the quantity of the glomerular
ultrafiltrate formed each minute in all
nephrons of the both kidneys
The normal value of GFR: 125 ml / min
Department of Physiology, Zhejiang University School of Medicine
Glomerular Filtration
Factors Affecting Filtration
1) The glomerular hydrostatic pressure
2) The colloid osmotic pressure of plasma
3) The Bowman’s capsule pressure
4) The renal plasma flow
5) Filtration area
6) Permeability of the filtration membrane
z
Factors that alter filtration pressure
change GFR
1. Glomerular hydrostatic pressure (PGC)
‹ systemic
blood pressure
‹ afferent
and efferent arteriolar
diameters
Blood lose, shock→ PGC ↓→NFP
↓→GFR↓
2. Capsular hydrostatic pressure
(PBS)
Renal
calculus,
tumor,
→PBS↑→NFP↓→GFR↓
3. The colloid osmotic pressure of plasma (πGC)
Ponderosus transfusion→ πGC ↓→NFP↑→GFR
↑
Glomerular Filtration
4. The renal plasma flow
a decrease in the rate of the oncotic pressure
the distance along the capillary in which
filtration was taking place
filtration
Factors governing GFR
‹ Factors
‹ Total
at the capillary bed are:
surface area available for filtration
‹ Filtration
‹ Net
membrane permeability
filtration pressure (NFP)
‹
Consequences of loss of protein in the urine:
‹ decrease
in osmotic pressure
‹ edema
‹ low
circulatory volume and possibly shock.
Loss of blood clotting proteins ： uncontrolled bleeding.
Loss of globulins and complement proteins make the
individual prone to infection.
Glomerular Filtration
z
The Glomerular Capillary Filtration Coefficient, Kf
9
The product of the hydraulic conductivity and
surface area of the glomerular capillaries
9
Kf = GRF/Net filtration pressure
Glomerular filtration rate (GFR)
2) Filtration fraction (FF)
The percentage of GFR in the renal plasma flow
Filtration fraction :
125/660＝19 %
Regulation of Glomerular
Filtration
‹
If the GFR is too high:
‹ Needed
substances cannot be reabsorbed quickly
enough and are lost in the urine
‹
If the GFR is too low:
‹ Everything
is reabsorbed, including wastes that
are normally disposed of
‹
GFR is used to evaluate the kidneys’ ability to
remove waste products from the body
‹
GFR is used to screen for:
Early signs of kidney damage
A coffee maker
Presence of protein in the urine is called proteinuria.
• Presence of blood cells in the urine is called hematuria.
Albuminuria
The presence of significant amounts of albumin in the urine.
The Uremic Syndrome
Homeostatic Disorder of water，
Electrolyte and Acid-alkali
Balance：
Volume Overload
Metabolic Acidosis
Hyperkalemia
Hyponatremia
Hypocalcemia
Hyperphosphatemia
Factors regulated by three mechanisms
renin-angiotensin-aldosterone system
Reabsorption and Secretion by the Renal
Tubules (buku yang diksh hal 643)
Reabsorption and Secretion by the
Renal Tubules
reabsorption (cat, buku yang diksh paragraf pertama hal
643)
180L/d
1.5L／d，
Normal urine volume: 1.5 L, >99％ reabsorbed , (<1%
excreted)
secretion：
Urine volume:
1.5L/d normal
(contains no RBC, no glucose bcs 100%
glucose are reabsorbed)
> 2.5 L polyuria
< 400 ml oliguria
< 100 ml anuria
(cannot be 0)
Renal handing of various plasma
constituents in a normal adult human
Reabsorption and Secretion by the Renal
Tubules
z
Mechanisms of tubular transport
1) Passive transport
(down their chemical or electrical gradient)
Simple diffusion
osmosis
facilitated diffusion
solvent drag:
the solutes dissolved in the water are also carried
along with the water.
Mechanisms of tubular transport
2) Active transport
‹ Primary
active transport
9 against an electrochemical gradient
9 directly requires metabolic energy (i.e.
hydrolysis of ATP)
Examples: Na+-K+ ATPase, H+ ATPase,
H+-K+ ATPase Ca+2 ATPase
Reabsorption and Secretion by the Renal
Tubules
‹ Secondary
active transport
‹ Symport
(Co-transport) Transported substances
move in the same direction across the membrane
Na+-glucose, Na+- amino acid
‹ Antiport
(Counter-transport) Transported
substances move in opposite directions across the
membrane
Na+-H+ antiport
Reapportion and Secretion by the
Renal Tubules
z
The pathway of reabsorption
1) Paracellular transport
9
9
9
9
5-10% of water transfer
Passive diffusion only
Requires favorable
electrochemical gradient
Passive diffusion of ions and large
non-polar solutes
2) Transcellular pathway
9
9
9
90-95% of water transfer
Passive transport
All active transport
the pathway of reabsorption
Apical
membrane
Paracelluar pathway
Basolateral
membrane
Basolateral
membrane
Transcelluar pathway
Reabsorption and Secretion by the
Renal Tubules
3) endocytosis
Uptake by cells of particles too large to diffuse through
the cell membrane
Example:
Reabsorption of filtered proteins in the proximal
tubules
Reabsorption by the Renal Tubules
(一)Na+、Cl- Reabsorption
1. Proximal tubule 70％
(1) Na+ and Clfirst half：active mechanisms
Na+: 65 ~ 70% absorbed
co-transport: Na+– glucose and amino acids
counter-transport: Na+– H+
Cl–: 55% absorbed passively
Proximal tubule
first half
co-transport: Na+– glucose and amino
acids
counter-transport: Na+– H+
Second half：Proximal tubule
Transcellular and paracellular
pathway
Transcellular
Na+ and Cl- co-transport ，
Na+-H+
Cl-／HCO3 counter-transport
Paracellular:
NaCl (Cl- by chamical gradient)
Water
hydrostatic pressure
(2)Water
Passive diffusion
osmotic
Transcellular and
paracellular
water channels：
aquaporin
(AQP-1)
（2003 Nobel prize）
blood
Tubular Reabsorption of Solutes and Water
Cl- goes up because
Na+ is reabsorbed
with glucose, amino
acids, Pi and HCO3Unchanged due
to isosmotic
reabsorption
Glucose, amino acids,
Pi and HCO3- go down
due to reabsorption
with Na+
2. Loop of henle
the thick ascending limb: Na+、Cl-：
Na+：2Cl-：K+ co-transport
Na+-H+ counter-transport
Na+、 Cl-、 K+：Transcellular and
paracellular
、 Cl：
the thick ascending limb: Na+
2、Loop
of henle
Clinic
furosemide （速尿)
inhibit cotransporter →NaCl reabsorbtion
osmolarity of the interstitial
water excretion
3、 Distal tubule and collecting ducts
Distal tubule：
Na+-Cl- symporter
↑\
Thiazide diuretics
Distal tubule and collecting ducts
pricipal cell (主细胞)
Na+ and water: amiloride
secretion：K+
intercalated cell (闰细胞)
reabsorbtion：HCO3secretion ：H+
Distal tubule
and collecting
ducts
CA:cabonic anhydrase
amiloride
Inhibite Na+ Channels
Distal tubule and collecting ducts
Water:
1) Isosmotic trasporting mechanism
a small amount in the early distal tubule
2) Counter-current mechanism
in the late distal tubule and collecting duct
controlled by ADH
Distal tubule and collecting ducts
Water：
AQP－2：apical membrane，VP(ADH)
AQP－3
Basolateral membrane
AQP－4
Acid-base balance
Acid-base balance
Acid-base balance
-
HCO3 and H+ transport
Acid-base balance
1、HCO3- reabsorbtion and H+ serection
（1）proximal：>80% HCO3- reabsorbtion
HCO3- : by CO2 reabsorbtion
H+分泌
Na+-H+ antiport
proton pump (H+-ATPase)
HCO3-
+
Na -HCO3
Cl -HCO3
1、HCO3- and H+
（1）proximal tubules：80%
（2）loop of henle：15%,
（3）distal tuble and collecting tuble：5%
proton pump
H+-K＋–ATP ase
CO2+H2O
HCO32HPO
H
PO
+
4
2
4
H
NH3
NH4+
HCO3- and H+ transport
NH3
glutaminase
glutamate +NH4+
Glutamine
glutamic dehydrogense
∂-ketoglutarate +NH4+
(2H+, 2HCO3- )
NH4+
NH3 + H+
Acid-base balance
Potassium
z the proximal tubule (65-70%)
z
z
z
Loop of henle(25-30%)
(key element)
in the distal tubule tubule and collecting
duct. (both secretion and reabsorbtion)
dependent on reabsroption of sodium,
under the control of aldosterone.
in competition with secretion of H+
Potassium
Tubular Reabsorption of Solutes and Water
4. Calcium
99% of filtered Ca+2 is reabsorbed
¾ Proximal tubule (60-65%), thick ascending loop of
Henle (25-30%):
passive and paracellular (favorable
electrochemical gradient)
4. Calcium
¾
Distal tubule & collecting duct (4-9%):
active and transcellular
‹Ca+2 diffuses down electrochemical gradient
at luminal membrane
‹Transported across basolateral membrane by
Na+-Ca+2 antiporter and Ca+2 ATPase
‹Regulation: parathyroid hormone,calcitriol
Tubular Reabsorption of Solutes and Water
5. Glucose
totally in the proximal
tubule, mainly the
early portions
Sodium-dependent
glucose transporter
Glucose
¾
Tm-G:
(the tubular transport
maximum for glucose)
¾
Renal threshold for
glucose
the critical value of the
plasma glucose
concentration when the
kidney begins to excrete
glucose
180 mg/dL
Glucose
¾
Renal threshold for glucose
the critical value of the plasma glucose concentration at
which the glucose first appears in the urine
180 mg/dL
‹
Maximal rate of transport of glucose (TmG)
plasma glucose concentration:300mg/100ml
375 mg/min (men), 300mg/min(women)
Glucose
Tubular Reabsorption of Solutes and Water
6. Amino acids
In a similar way as glucose but by different carrier
Urinary Dilution and Concentration
Urine volume: 1.5L/d normal
> 2.5 L /d polyuria
< 400 ml /d oliguria
< 100 ml/d anuria
osmolality :
50-1200 mOsm/(kg.H2O)
> plasma hyperosmolality urine
= plasma
< plasma hypoosmolality urine
location：Loop of henle
Urinary concentrating mechanism
¾
¾
Corticomedullary
concentration gradient
A gradient of
increasing osmolality
Urinary concentrating mechanism
¾
The countercurrent exchanger in the kidney
Urinary Dilution and Concentration
‹ Urinary
concentrating
mechanism—the
countercurrent theory
¾
The countercurrent
multiplication
Urinary concentrating mechanism
¾
The countercurrent exchanger in the kidney
Permeability properties of the tubular system
Portions of the tubular
system
Water
Sodium
Urea
Thick ascending limb of
Henle’s loop
impermeable
Actively transport
impermeable
thin ascending limb of
Henle’s loop
impermeable
Highly permeable
mid permeable
thin descending limb of
Henle’s loop
highly permeable
impermeable
impermeable
the distal tubule
highly permeable in the
presence of ADH
secretion of H+ in the
presence of aldosterone in
exchange for Na+
impermeable
the collecting duct in the
cortical and outer medulla
highly permeable in the
presence of ADH
highly permeable
impermeable
the collecting duct in the
inner medulla
highly permeable in the
presence of ADH
highly permeable
highly permeable
Urinary concentrating mechanism
¾
The countercurrent exchanger in the kidney
Urinary concentrating mechanism
¾
Establishing of osmotic gradient of the renal medulla
Urinary concentrating mechanism
¾
Maintenance of the osmotic gradient in the medulla
Urinary concentrating mechanism
¾
The countercurrent
exchange
Operation of the vasa recta as
countcurrent exchangers in the kidney
NaCl and urea diffuse out of the ascending limb of the
vessel and into the descending limb,whereas water
diffuses and into the ascending limb of the vascular loop
Urinary concentrating mechanism
¾
Corticomedullary
concentration gradient
Urinary Dilution and Concentration
‹
9
9
Formation of concentrated or dilute urine
In the presence of ADH, which increases the
permeability of the collect duct to water, water is
drawn from the lumen into the interstitial fluid,
that results in the excretion of a concentrated
urine
In the absence of ADH, the dilute renal fluid is
excreted
Urinary Dilution and Concentration
‹ Factors
that affect the concentration and
dilution of the urine
1) Damage of renal medulla
result in an impairment of the concentrating ability
2) Loop diuretics
such as frusemide, inhibit the active transport of
NaCl at the thick asending portion of Henle’ loop,
interfere with the establishiment of the osmotic
gradient in the medulla of the kidney
Urinary Dilution and Concentration
3) Lack of urea in the body
such as malnutrition, reduce the osmotic gradient
established in the renal medulla
4) Increased velocity of blood flow in the vasa recta
upset the osmotic gradient in the medulla by
carrying away amount of NaCl, thus reducing the
osmotic gradient
Control of Renal Functions
‹Autoregulation
osmotic diuresis
glomerulotubular balance
‹Nervous Control of Renal Functions
renal sympathetic
‹ Hormonal Control of Renal Functions
Renin-angiotensin system
vasopressin
osmotic diuresis
‹ The
presence of large quanties of
unreabsorbed solutes in the renal tubules
causes an increase in urine volume called __
‹ Solutes that are not reabsorbed in the
proximal tubules exert an appreciable
osmotic effect
osmotic diuresis
the concentration of unreabsorbed solutes in the
tubules↑→isotonic fluid→
water reabsorption ↓→ Na+ reabsorption↓→
urine volume↑，
excretion of NaCl ↑
diabetes（glucose）
mannitol→ isotonic fluid →diuresis
glomerulotubular balance
1. Conceptor：GFR ↑→
an increased reabsorption of solutes and water in the
proximal tubule
2. Mechanism: in general the percentage of the solute
reabsorbed is held constant despite variations in
GFR
constant fraction reabsorption
（65-70% of GFR ）
glomerulotubular balance
GFR↑
The protein in the glomerular capillary plasama
the oncotic pressure in the peritubular capillaries↑
↓
solute and fluid into peritubular capillaries
Na+ reabsorption ↑
G-T balance
3. Meaning： the percentage of the
solute in urine is held constant
G-T balance is to reduce the impact
of GFR changes on the amount of
Na+ and water excreted in the urine
Nervous Control of Renal Functions
Renal sympathetic nerve
1. α-R→arterioles contracts→ RBF↓→GFR↓
2. Proximal tubule α-R→Na+、water reabsorption↑
3. juxtaglomerular cellsβ-R→Renin↑→
Na+、water reabsorption↑
Hormonal Control of Renal Functions
‹vasopressin, VP
‹Renin-angiotensin system
‹atrial natriretic peptide, ANP
‹ Kallirein and kinin system
‹ endothelin ET
‹ nitric oxide
‹catecholamine
‹ Prostaglandin E
Hormonal Control of Renal Functions
‹ Antidiuretic
hormone (ADH)
acts on the kidneys to regulate the volume and
osmolarity of the urine
9
9
Peptide hormone, increasing water permeability
of collecting duct
ADH
diuresis
ADH
antiduresis
Insertion of aquaporins in apical membrane
Antidiuretic hormone (ADH)
Paraventricular
Supraoptic nucleus
Posterior
pituitury
Hormonal Control of Renal Functions
There are two effective
stimuli that change ADH
release.
9
9
One is plasma osmolality
plasma
osmolality↑
→→
hypothalamic
osmoreceptors
→→ production and release of
ADH ↑
the other is blood volume
Hormonal Control of Renal Functions
9
the other
volume
is
blood
blood volume ↓
→→ baroreceptor reflex & atrial
stretch receptors
→→ vagus nerve
→→ brainstem(NTS)
→→ ADH release ↑
Water diuresis
Water diuresis
plasma
osmolality
→→
hypothalamic osmoreceptors →→
production and release of ADH
Hormonal Control of Renal Functions
‹ Aldosterone
9
9
secreted by the glomerulosa of the adrenal cortex
Increases the reabsorption sodium in the distal
tubule and early collecting duct
¾
¾
Increases number of Na+ channels
Increases number activity of Na+ pumps
The reabsrption of sodium is coupled to secretion of
potassium.
Hormonal Control of Renal Functions
‹
a.
b.
c.
d.
Regulation of Aldosterone secretion
Renin-angiotensin system
Plasma concentrations of sodium and potassium
Extracellular fluid volume
Adrenocorticotrophin (ACTH)
Renin-angiotensin system
Renin-angiotensin system
Renin-angiotensin system
Atrial natriuretic peptides (ANP)
‹Involved in control of both salt and water balance
‹Stretch-sensitive cells in wall of atrium
‹Stimulated by stretch to secrete ANP
‹ANP
Atrial natriuretic peptide (ANP)
•Produces natriuresis and
diuresis
•Decreases renin release
•Reduces total peripheral
resistance via
vasodilatation
•Decreases heart rate,
cardiac output
Endothelium-derived vasoactive substances
•Vasodilator factors
PGI2-prostacyclin
EDRF, NO-endothelium-derived
relaxing factor, nitric oxide
EDHF-endothelium-dependent
hyperpolarizing factor
The 1998 Nobel Prize in Physiology or Medicine
Nitric oxide as a signaling molecule in the
cardiovascular system
Louis J Ignarro
Ferid Murad
Robert F Furchgott
NO, a signaling molecule with potent cardiovascular, immunomodulatory
& neuromediatory activities (Bredt, 1994)
•Vasoconstrictor factors
Endothelin
Kinin & histamine
Bradykinin, Kallidin--Plasma
Histamine--Mast cells in response to injury, inflammation,
and allergic responses
Similar effects:
causes vasodilatation
increases capillary permeability
Prostaglandins
Hormonal Control of Renal
Functions
‹ Epinephrine
and norepinephrine
‹ Prostaglandin
‹ Adrenomedullin
‹ Parathyroid hormone, PTH
Renal Clearance
Cx =
Cx =
Ux * V
UxPx
*V
Px
Renal Clearance
z
Defined as the volume of plasma required to
supply the amount of a substance X to be excreted
in urine per unit time
Micturition
‹ Micturition
reflex
Micturition occurs when the
intravesicular pressure reaches
70 cmH2O via a reflex action
Pdet, cm H2O
50
0
0
volume
300 ml
detrusor
Micturition
‹ Higher
control of micturition
There are inhibitory and facilitatory centers in the
cerebral cortex and pons
Micturition
Micturition reflex.swf
Micturition mechanism.swf
Abnormality of micturition
Injure
‹ affrent nerve →overflow incontinence
‹ effrent
nerve
→ urine retention
‹ spinal
cord
spastic neurogenic bladder