REGULATION OF WATER &

ELECTROLYTES BALANCE

by:
Husnil Kadri

Biochemistry Departement
Medical Faculty Of Andalas University
Padang
Maintenance of Blood Pressure Homeostasis
Angiotensin Pathway**
 Regulation of Water**
The hypothalamic thirst center is
stimulated:
By a decline in plasma volume of 10%15%
(mknsme AT2 slh stuny)
By increases in plasma osmolality of 12%
Via baroreceptor input (jk trhmbt), angiotensin
II, and other stimuli
 Osmoregulation**
Osmoreceptors:
Increase in plasma osm--> hypothalamus
stimulated to release ADH (hypothalamic
set point 285 mOsm/L solution)
Respond to < 2% change in plasma
osmolarity
 Regulation of Water
Thirst is quenched as soon as we begin to
drink water
Feedback signals that inhibit the thirst
centers include:
Moistening of the mucosa of the mouth and
throat (krongkongn cs)
Activation of stomach and intestinal stretch
receptors
 Regulation of Water Loss
Obligatory water losses include:
Insensible water losses from lungs and skin
Water that accompanies undigested food
residues in feces
Obligatory water loss reflects the fact that:
Kidneys excrete 900-1200 mOsm of solutes
to maintain blood homeostasis
Urine solutes must be flushed out of the body
in water
 Regulation of ADH
Factors that specifically trigger ADH
release include:
prolonged fever; excessive sweating,
vomiting, or diarrhea; severe blood loss;
and traumatic burns.

Dr distal dst, jg pngaruhi reab na/krj aldos

(saling), o/ aquaporin2 d lumen, 3&4 kluar
tubuli
Regulation of ADH
 Disorders of Water Balance:
Dehydration

Causes include: hemorrhage, severe

burns, prolonged vomiting or diarrhea,
profuse sweating, water deprivation(tnpa
mnum) , and diuretic abuse (wrng/bad
use/treatment)
Signs and symptoms: cottonmouth, thirst,
dry flushed skin, and oliguria (urin sdkt)
Other consequences include hypovolemic
shock and loss of electrolytes
 Disorders of Water Balance:
Edema
Atypical accumulation of fluid in the
interstitial space, leading to tissue swelling
(mmbsar)
Caused by anything that increases flow of
fluids out of the bloodstream or hinders
(sulit trjdi) their return
 Edema
Hindered fluid return usually reflects an
imbalance in colloid osmotic pressures
Hypoproteinemia low levels of plasma
proteins
Forces fluids out of capillary beds at the
arterial ends
Fluids fail to return at the venous ends
Results from protein malnutrition, liver
disease, or glomerulonephritis
 Edema
Blocked (or surgically removed) lymph
vessels:
Cause leaked proteins to accumulate in
interstitial fluid
Exert (pngaruhi) increasing colloid osmotic
pressure, which draws fluid from the blood
Interstitial fluid accumulation results in low
blood pressure and severely impaired
circulation
Transportasi kelebihan cairan intersisial ke
aliran darah (fngsi lymph)
 Electrolyte Balance

Electrolytes are salts, acids, and bases,

but electrolyte balance usually refers only
to salt balance
Salts enter the body by ingestion and are
lost via perspiration (bkrngat), feces, and
urine
 Sodium in Fluid and Electrolyte
Balance**
Sodium salts:
Account for 90-95% of all solutes in the ECF
Contribute 280 mOsm of the total 300 mOsm
ECF solute concentration
Sodium is the single most abundant (bnyk)
cation in the ECF
Sodium is the only cation exerting significant
osmotic pressure
 Sodium Reabsorption:
Primary Active Transport
Sodium reabsorption is almost always by
active transport
Na+ enters the tubule cells at the luminal
membrane
Is actively transported out of the tubules by a
Na+-K+ ATPase pump
Di tcp na nh4+ countertrans ad
 Sodium Reabsorption:
Primary Active Transport
From there it moves to peritubular
capillaries due to (karena):
Low hydrostatic pressure (blood)
High osmotic pressure of the blood
Na+ reabsorption provides the energy and
the means for reabsorbing most other
solutes
 Regulation of Sodium Balance:
Aldosterone
Sodium reabsorption
65% of sodium in filtrate is reabsorbed in the
proximal tubules
25% is reclaimed in the loops of Henle (thick
asc) (na.2k.cl, d reab sklgus cek gmbr)
3Na ca+ countertrans d distal ad jg
When aldosterone levels are high, all
remaining Na+ is actively reabsorbed
 Regulation of Sodium Balance:
Aldosterone**
Adrenal cortical cells are directly
stimulated to release aldosterone by
elevated K+ levels in the ECF
Aldosterone brings about its effects
(diminished urine output and increased
blood volume) slowly (o/ gsk-38 pd gmbr/
pengaruhi aqp2 scr lngsng)
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Atrial Natriuretic Peptide (ANP)
Reduces blood pressure and blood
volume by inhibiting:
Events that promote vasoconstriction
Na+ and water retention (u/ tbuh/reabs)
Is released in the heart atria as a response
to stretch (elevated blood pressure)
Has potent diuretic and natriuretic effects
Promotes excretion of sodium and water
Inhibits angiotensin II production
BP turun
Mechanisms and Consequences of ANP Release
 Regulatory Site Of Potassium:
Cortical Collecting Ducts
Less than 15% of filtered K+ is lost to urine
regardless (krg rspect/attention) of need
K+ balance is controlled in the cortical
collecting ducts by changing the amount of
potassium secreted into filtrate
When K+ levels are low, the amount of
secretion and excretion is kept to a
minimum
K+ ad yg cotrans cl- d tcp&henle
 Influence of Aldosterone**
Aldosterone stimulates potassium ion
secretion by principal cells
In cortical collecting ducts, for each Na+
reabsorbed, a K+ is secreted
Increased K+ in the ECF around the
adrenal cortex causes:
Release of aldosterone
Potassium secretion
Pompa dr tubuli ke luar, protein transport dr
tubuli ke lumen
Potassium Balance
Renal Potassium Handling
 Regulation of Calcium and Phosphate
PTH promotes increase in calcium levels by
targeting:
Bones PTH activates osteoclasts to break down
bone matrix
Small intestine PTH enhances(bgus dlam)
intestinal absorption of calcium
Kidneys PTH enhances calcium reabsorption and
decreases phosphate reabsorption
D tcp u/ metab vit D, vit D u/ aktvn calbindin tcd
Calcium reabsorption and phosphate excretion
go hand in hand
Ca&mg space d p,h,d sdngkn, po4 cotrans
2na+ d p,d,c
Regulation of Calcium and Phosphate
Filtered phosphate is actively reabsorbed in
the proximal tubules
In the absence of PTH, phosphate
reabsorption is regulated by its transport
maximum and excesses are excreted in urine
High or normal ECF calcium levels inhibit PTH
secretion
Release of calcium from bone is inhibited
Larger amounts of calcium are lost in feces and
urine
More phosphate is retained
 Influence of Calcitonin

Released in response to rising blood calcium

levels
Calcitonin is a PTH antagonist, but its
contribution to calcium and phosphate
homeostasis is minor to negligible
 Regulation of Anions
Chloride is the major anion accompanying
sodium in the ECF
99% of chloride is reabsorbed under
normal pH conditions (di normal pH)
When acidosis occurs, fewer chloride ions
are reabsorbed
Other anions have transport maximums
and excesses are excreted in urine
Calcium, phosphate, and magnesium metabolism**
Hereditary disorders of tubular transport
Disorders of sodium and water metabolism
Hyponatremia and hypernatremia**,
seizure=illnes, excess=klbhn
 Reference

1. Ivkovic, A and Dave, R. Renal review. ppt. 2008

2. Marieb, EN. Fluid, electrolyte, and acid-base balance. ppt.
Pearson Education, Inc. 2004
3. Marieb, EN. The urinary system part B. ppt. 2004.
4. Silverthorn, DU. Integrative Physiology II: Fluid and Electrolyte
Balance. Chapter 20, part B. ppt. Pearson Education, Inc. 2004

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