You are on page 1of 5

Physiology 4.

7

H2O & Electrolytes Regulation, Micturition
Reflex & Urinalysis

Nov 23, 2011
Dr. Carolina C. Jerez

OUTLINE
WATER AND ELECTROLYTE REGULATION
I.
Effects of sodium reabsorption
II.
Blood pressure regulation
III.
Potassium regulation
IV.
Factors maintaining the tonicity of the medullary interstitium
V.
Plasma osmolarity regulation
MICTURITION REFLEX
I.
Micturition contraction
II.
Control of brain in micturition
URINALYSIS
I.
Macroscopic examination
II. Microscopic examination
Add’l info from Berne and Levy in Times New Roman (bold)

WATER AND ELECTROLYTE REGULATION
I. EFFECTS OF SODIUM REABSORPTION




Creates an osmolarity favoring the reabsorption of water
Helps prevent excessive water loss in the stool
Nutrients, phosphates, sulfates are also reabsorbed
Achieves hydrogen ion secretion
Chloride reabsorption – excessive chloride secretion can cause
diarrhea

Figure 1. Role of Renin

Table 1. Different Effcets of Angiotensin II

II. BLOOD PRESSURE REGULATION
 One function of the kidney
 Set Point: value of BP at any given time (depending on the
individual’s activity)
 Detectors – to determine the changes in BP
 Signals generated in response with each changes
 Effectors – supposed to bring back BP to normal
Ex. Compensatory mechanism

RESPONSES TO CHANGES IN BP
 Short term: Baroreceptor reflexes (detect changes in the amount
of blood in the body passing through the specific area)
 Intermediate:
o Renin
 Secreted when there is low BP and detected by the granular
cells (which also secretes renin)
 Needed in the conversion of angiotensinogen which comes
from the liver to become Angiotensin I  Angiotensin II in
the lungs in the presence angiotensin converting enzyme
which is the ACE (Fig 1)
 Renin-angtiotensin is an intermediate compensatory
mechanism for changes in blood pressure
 Regulator of Na+ and K+ balance
o Macula Densa cells will detect the amount of fluid and sodium
chloride flowing through the juxtamedullary apparatus
 What will be the main effect of angiotensin II?
o It is a vasoconstrictor agent and thus changes total peripheral
resistance  increase blood pressure
o Stimulates the release of aldosterone and antidiuretic hormone
(ADH)  long term response to changes in blood pressure
(Figure 2)
Figure 2. Effects of Angiotensin II
Group 5 | Ballero, Baluyot, Bamba, Bañas

Page 1 of 5

 Long term: Renal regulation of water and NaCl
o ALDOSTERONE from adrenal glands
 Stimuli for the release of aldosterone: Presence of ACTH
(Adrenocorticotrophic Hormone), Angiotensin II, and an
increase of plasma Potassium
 Effects : Increase sodium and fluid retention (increase
reabsorption of sodium in the distal collecting tubule, CT and
ducts)
o ADH (Antidiuretic Hormone) from the Posterior Pituitary
Gland
 Ways of releasing ADH – stimulating either the baroreceptor
and the osmoreceptor
 Effects of ADH: Increase water permeability in areas in which
it is not permeable (DT but primarily in the cortical and outer
medullary areas of the CT and ducts). ADH is also a
powerful antidiuretic, increasing water reabsorption and
reducing urine excretion.
 The mechanism by which ADH is able to increase water
reabsorption will be the increase of water channels
(Aquaporin II). So with an increase of water and sodium
reabsorption able to maintain a normal blood volume and
a new set point for blood pressure.
o Atrial Natriuretic Hormone/Factor (ANH/ANF)
 Released from Atrium when there is an increase volume in
atria (inc blood volume)
 Effect is inc in naturesis inc sodium excretion




+

+

High K diet (avocado and baby carrots)  inc K secretion
+
+
Low K diet  dec K secretion
+
+
K - sparing diuretic  dec K secretion
During diuretic therapy:
+
o K gets out of the cell and into the lumen  excreted in the
urine  can cause hypokelemia
+
o K -sparing diuretics are use to prevent hypokalemia

IV. FACTORS MAINTAINING TONICITY IN THE
MEDULLARY INSTERSTITIUM
A.COUNTERCURRENT MULTIPLIER SYSTEM

Figure 5. Countercurrent Multiplier System

Figure 3 . Summary of the Regulation of Sodium and Water by aldosterone,
ADH, and ANH

III. POTASSIUM REGULATION

 Critical for concentrating a person’s urine
 Repetitive reabsorption of NaCl by the thick ascending loop of
Henle and continued inflow of new NaCl from the proximal tubule
into the loop of Henle
 NaCl reabsorption at the ascending limb establishes a
concentration gradient between the interstitium and ascending
limb of the loop of Henle of 200 mili-osmole
o The descending limb and the interstitium will have the same
osmolarity but a 200 mili osmol difference for the ascending
and descending limb
 Why? Because of the slow blood flow in the medullary area
 not all sodium which gets out of the interstitium can be
reabsorbed right away  NaCl will stay in the interstitium 
maintaining the osmolarity in the medulla
 No medulla  no reabsorption of water (passive reabsorption
of water)
o In the presence of ADH
 more water reabsorption in the collecting tubules and more
concentrated urine
 more NaCl reabsorption in the ascending limb

B. VASA RECTA
 Peritubular capillaries that go down with the loop of Henle in the
medullary area, supplying blood and nutrients to the renal
medulla. Also highly-permeable to solute and water via AQP1
and works at the same time to move excess solute and water
out
Figure 4 . Potassium handling
Group 5 | Ballero, Baluyot, Bamba, Bañas

Page 2 of 5

 Descending limb of vasa recta:
o Solute goes IN since fluid inside the vasa recta is less tonic than
outside
o Water moves OUT since the intertitium has a higher osmolarity
 Ascending limb of vasa recta
o Solute goes OUT since fluid inside the vasa recta has higher
osmolarity
o Water moves IN in response to the increased osmolarity from
the descending limb
 Therefore this is an EXCHANGER so that the osmolarity will not
vary so much  maintaining the tonicity of the medullary area

MICTURITION REFLEX
 Also known as urination, voiding or peeing.
 Micturition center is in the the rostral pons, specifically the
Barrington’s Center
 It is the process of disposing urine from the urinary bladder via
the urethra
 Full bladder felt at 200-300 mL  Trips mechanoreceptors that
are eventually triggered by the pressure, resulting in discharge
 Normally under voluntary control but may occur involuntarily
especially in infants, elderly and those with neurologic injuries
 Involves coordination of the central, autonomic and somatic
nervous systems
I. MICTURITION CONTRACTION
 Product of stretch reflex from the sensory stretch receptors found
in the bladder wall
 Receptors in the posterior urethra also have an influence in the
production of contractions
 Signals from stretch receptors →sacral segments of the spinal
cord via pelvic nerves→ back to the bladder via parasympathetic
nerve fibers

Figure 6. Countercurrent Exchange in the Vasa recta

C. UREA
 product of protein metabolism
 is really filtrable, 50% of urea will be reabsorbed in the PCT; 50%
in the tubular lumen
 the distal tubule, cortical collecting ducts and the outer medullary
collecting ducts are IMPERMEABLE to urea; thus no urea is
reabsorbed in these segments
 ADHinc urea permeability of the inner medullary collecting
ducts into the insterstitial fluid contributes to urea recycling
 Urea secretion varies with urine flow rate (UFR)
o High water reabsorption (low UFR)  greater urea
reabsorption and dec urea excretion
o Low water reabsorption (high UFR)  less urea reabsorption
and inc urea excretion

V. REGULATION OF PLASMA OSMOLARITY
 Accomplished by varying the amount of water excreted relative to
the amount of solute excreted ( i.e., by varying the urine
osmolarity.

A. RESPONSE TO WATER DEPRIVATION
 water deprivation  inc plasma osmolarity  stimulates
osmoreceptors  inc secretion of ADH  inc water permeability
of late distal tubule and collecting duct  inc water reabsorption
 INC urine osmolarity and DEC urine volume  DEC plasma
osmolarity toward normal

B. RESPONSE TO INTAKE
 water intake  dec plasma osmolarity  inhibits osmoreceptors
 dec secretion of ADH  dec water permeability of late distal
tubule and collecting duct  dec water reabsorption  DEC urine
osmolarity and INC urine volume  INC plasma osmolarity
toward normal
Group 5 | Ballero, Baluyot, Bamba, Bañas

Figure 7. Urinary Bladder Fullness Sensation
Note: The detrussor muscle contracts while the urethra and pelvic floor
relaxes at the emptying phase to initiate micturition

 Bladder only partially filled.
o Contractions usually relax spontaneously
o Contraction of detrussor muscle ceases
o Results to pressure going back to baseline
 Bladder gradually fills up
o Micturition reflex becomes more frequent
o Detrussor muscle produces greater contractions
o Pressure in the urinary bladder is low during filling (5 to 10 cm
H2O), but it increases abruptly when micturition begins
 Important: Micturition reflex is self regenerative
o Initial contraction of bladder activates stretch
receptors→production of greater impulses to the bladder and
posterior urethra
o This then results to further increase in the reflex contraction of
the bladder
o Becomes a cycle until bladder reaches a strong enough degree
of contraction
 After a few seconds to more than a minute, the reflex fatigues
and the cycle ceases →bladder relaxes
 Thus the reflex is a single complete cycle of:

Page 3 of 5

Progressive and rapid increase in pressureA period of
sustained pressureReturn of pressure to the basal tone of
the bladder
 If a reflex occurs but is not followed by successful bladder
micturition, the nervous components of the reflex remain
inhibited for a few minutes to one hour or more prior to
occurrence of another reflex
 As the bladder continues to fill up with urine, the reflex occurs
more frequently and more powerfully
o If it is powerful enough, it causes another reflex
 Reflex passes through the pudendal nerves to the external
sphincter to inhibit it
 If inhibition is more potent in the brain than voluntary
control, urination will occur
o If this is not so, the bladder will continue to fill up with urine
until the reflex becomes powerful enough to cause urination.
II. ROLE OF BRAIN IN MICTURITION
 Micturition is a completely autonomic spinal cord reflex but can
be inhibited or facilitated by brain centers
 Brain centers include:
o Brain stem mainly in the pons (facilitate and inhibitory centers)
o bladder afferent fibers excite neurons that project to the
brainstem and activate the micturition center in the rostral
pons (Barrington's center)
o Cerebral cortex (mainly inhibitory but some excitatory)
 Reflex is the basic cause of micturition but higher centers exert
final control
o These higher centers keep the reflex partially inhibited except
when micturition is desired
o Higher centers can also prevent micturition even if the reflex
occurs
 This is via the continual tonic contraction of the external
bladder sphincter until a convenient time is available
 When the time is right, cortical centers facilitate sacral micturition
centers initiating the reflex at the same time producing inhibition
of the external urinary sphincter

Figure8. Brain Control in Micturition
Note: Brain centers include the pontine micturition center, periaqueductal
gray and cerebral cortex.

 VOLUNTARY URINATION
o Pressure in the bladder contracts abdominal muscles
o Pressure in the bladder increases; extra urine enters bladder
neck and posterior urethra
o Walls of the bladder and posterior urethra stretch
o Stretch receptors stimulated
Group 5 | Ballero, Baluyot, Bamba, Bañas

o Micturition reflex excited with simultaneous inhibition of
external urethral sphincter
o Urination

I.

URINALYSIS
MACROSCOPIC EXAMINATION

 Most Ideal sample: early morning urine (since it is the most
concentrated); get midstream urine
 Normal urine is typically light yellow and clear without cloudiness
 An important and routine tool for detecting disease

A.PHYSICAL CHARACTERISTICS
 Volume : 600-2000 ml /day (She explicitly said she would go with
500-2000 ml/day)
o Oliguria : decrease in the normal volume of urine
o Polyuria : increased in normal urine volume
 Color : colorless –black
o Pale yellow, straw, light yellow, dark yellow, amber
o If your taking medicines, there will be changes in the urinehighly colored
 Appearance refers to clarity of the urine
o Freshly voided urine is clear
o Cloudiness due to amorphous phosphates and carbonates
o Turbidity may be due to the presence also of: WBC, RBC,
Epithelial Cells, Bacteria
 Specific gravity: determines how dilute or concentrated the urine
o Density of a substance compared with a similar volume of
distilled water at a similar temperature
o Can be determined using dipstick or urinometer
o Normal Value = 1.010 to 1.025 (higher value = more
concentrated)
 Odor: faintly aromatic  usually due to the breakdown of urea

B.CHEMICAL ANALYSIS
Urine chemical dipstick analysis - narrow plastic strip with squares of
different color attached to it. Strip is dipped into the sample and the
color changes will take place and be interpreted accordingly (think
pH paper)
 pH: 4.5-8
o Acidic Urine: due to high meat or high protein and cranberry
juice (Uric acid will precipitate in acidic urine)
o Alkaline Urine: Vegetarian diets (Phosphates will precipitate in
alkaline urine)
 Protein in the urine is most indicative of renal problem (signifies
that high molecular weight substances have passed through the
glomerular filtration barrier; more sensitive to albumin than other
globulins). Higher than trace amounts of protein is usually
indicative of disease.
o N.V.: 10 mg/dl or 100 mgs /24 hours
o Microalbuminuria: proteinuria that cannot be detected by
reagent strips (Significant if 30-300 mgs/24 hrs.)
o Orthostatic Proteinuria:
 Caused by High fever, Exposure to cold, Strenuous exercise,
Dehydration, Acute phase of severe illness
 Blood in the Urine:
o Hematuria: RBC in urine
 Causes: Renal calculi (renal stones), glomerulonephritis,
pyelonephritis, tumors, trauma, exposure to toxic chemicals,
strenuous exercise
 Glucose: indicates that filtered load of glucose exceeds the
maximal tubular capacity for glucose. In diabetes mellitus, urine

Page 4 of 5



testing for glucose is often substituted for blood glucose
monitoring
Ketones: detects acetoacetic acid only. In ketoacidosis (insulin
deficiency or deprivation), it can be present in large amounts in
urine before elevated in plasma
Nitrite: Positive in bactenuria caused by gram negative bacteria
which produce nitrate reductase enzyme
Bilirubin: indicates presence of liver disease or biliary obstruction.
Very low levels of bilirubin can be detected in urine even when
serum levels are below clinical detection of jaundice.
Urobilinogen : increased in any condition that causes an increase
in production or retention of bilirubin

II. MICROSCOPIC EXAMINATION
 In a centrifuge urine sample, look for
o Formed elements (RBC, WBC, Epithelial Cells)
o Bacteria
o Crystals
o Casts: formed in the lumen of the Distal Convoluted Tubules
(DCT) and Convoluted Tubules (CT)
 TYPES: Hyaline, Red cells, WBC casts, Bacteria, Epithelial cell,
Granular
Table2. Normal Urine Constituents Excreted (in g/24 hrs)
Urea
25-30
Sodium
1-5 (NaCl-15.0)
Uric Acid
0.6-0.7
Potassium
2-4
Creatinine
1.0-1.2
Calcium
0.2-0.3
Hippuric Acid
0.7
Magnesium
0.1
Ammonia
0.7
Chloride
7
Amino Acids
3
Phosphate/Sulfate
1.7/1.8-2.5

Group 5 | Ballero, Baluyot, Bamba, Bañas

Page 5 of 5