The document discusses the regulation of body fluids and osmolality, emphasizing the kidneys' crucial role in maintaining extracellular fluid volume to ensure proper blood pressure and tissue perfusion. It details the osmoreceptor-ADH system and thirst mechanism as primary regulators, along with the effects of various hormones such as aldosterone and atrial natriuretic peptide on sodium and water balance. Additionally, it covers clinical implications of conditions like hyponatremia and hypernatremia related to water and sodium imbalances.

1. z
REGULATION OF BODY
FLUIDS and osmolality
RENAL
PHYSIOLOGY

2. z
Introduction
It is important to
regulate ECF volume to
maintain BP, essential
for adequate tissue
perfusion and function.
Changes in extracellular
volume cause changes
in the cell volume that
compromise the
function of cell
especially in the CNS.
Regulation of body
fluids and osmolality is
an integrated function of
various organ systems.
Kidneys play a major
role.

4. z
Tonicity- the osmolality of a solution relative to
plasma
§ Osmolality- It is the number of osmoles per kilogram of
solvent
§ Normal plasma osmolality: 290 mosm/l
Na+
HCO3-
Cl-
Glucose
urea
94% of extracellular osmoles
3-5% of total osmoles

5. Normal ECF and ICF concentration table

7. TWO PRIMARY
SYSTEMS
INVOLVED IN
REGULATION OF
BODY FLUIDS-
Osmoreceptor-ADH
system(water excreting)
The thirst
mechanism(water intake)

8. OTHER
MECHANISMS
for regulation
RAAS system
Natriuretic
hormones

9. Osmoreceptor- ADH feedback system
Osmolarity increases above normal because of water
deficit-
1. Osmoreceptor cells, in the anterior hypothalamus near the
supraoptic nuclei, shrink because of increase in the ECF
osmolarity.
2. Osmoreceptors send signals to additional nerve cells in the
supraoptic nuclei which relay signals to posterior pituitary.

10. 3. Aps in the posterior pituitary stimulate release of
ADH
§ ADH enters blood stream and transported to
kidneys
§ In kidneys it increases the water permeability of
late DCT, cortical collecting tubules and medullary
collecting ducts.
§ This results in the increased water reabsorption
and excretion of a small volume of concentrated
urine.

11. Water deficit
Extracellular osmolarity
ADH secretion
Plasma ADH
H2O permeability in distal tubules
Collecting tubules
H2O reabsorption
H2O excreted

12. Other
Stimulation
OF ADH
ADH release is also controlled by
cardiovascular reflexes that respond to-
1. Decrease in BP
2. Decrease in blood volume(including
Arterial baroreceptor reflexes &
Cardiopulmonary reflexes)
3. Other stimuli to CNS e.g. nausea
4. Drugs(nicotine and morphine) and
hormones
5. Alcohol inhibits ADH release

13. THIRST CONTROLLING MECHANISM
Fluid intake is regulated by
thirst mechanism, which,
together with osmoreceptor
ADH mechanism, maintains
control of extracellular fluid
concentration.

14. Central nervous system CENTERS FOR THIRST
Anteroventral wall of the
third ventricle
anterolaterally in the
preoptic nucleus when
stimulated electrically
causes immediate drinking
that continues as long as
the stimulation lasts.

15. z Decreased volume of ECF Increased plasma osmolality
Decreased saliva secretion
Stimulates
osmoreceptors
in hypothalamic
thirst centre
Dry mouth
Sensation of thirst
Person seeks a drink
Water absorbed from GIT
Decreased osmolality of
ECF
Increased volume of
ECF
Stimulate
Inhibit

16. z
Stimuli for
thirst
§ sed ECF osmolarity
§ sed ECF volume and
arterial pressure
§ Angiotensin II & III
§ Dryness of mouth and
mucous membranes
of esophagus
§ Degree of gastric
secretion
OTHER
FACTORS
(SHORT
LIVED)

17. Summary

20. URINE OUTPUT
WATER
REABSORPTION
SODIUM
REABSORPTION
E.C.F
CAPILLARY
PRESSURE & LONG
TERM INCREASE IN
ARTERIAL PRESSURE

21. Role of ANGIOTENSIN II
When sodium intake is elevated above normal, renin
secretion is decreased, causing decreased angiotensin II
formation, thus increasing the kidneys’ excretion of sodium
and water
The net result is to minimize the rise in extracellular fluid
volume and arterial pressure that would otherwise occur
when sodium intake increases.
Changes in activity of the renin-angiotensin system act as
a powerful amplifier of the pressure natriuresis mechanism
for maintaining stable blood pressures and body fluid
volumes.
01
02

22. z
Role of aldosterone in ecf
regulation
Ø It is the principal regulator of Na+
absorption
Ø It works in cells of cortical collecting
duct.
Ø Na+ reabsorption in this part of renal
tubule accounts for only 2% of total
Na+ reabsorption
Ø Aldosterone saves salt.
Ø It works to increase Na+ reabsorption
by promoting he expression of all the
channels and pumps depicted in the
figure.

23. z
ATRIAL NATRIURETIC
PEPTIDE
A small peptide produced from
the right atrial wall as a result of
atrial stretching due to
hypervolemia.
Acts to increase Na excretion by
increasing GFR and blocking Na
reabsorption in the proximal
collecting duct.
Water elimination(increased urine
output)
Increased diuresis
Decreased blood volume and
blood pressure

24. APPLIED
clinical correlation
Dehydration
Overhydration

26. HYPONATREMIA
§ Hyponatremia is defined as a plasma Na+ concentration <135
mEq/L.
§ It is due to a relative excess of water in relation to sodium.
§ It can result from excessive loss of sodium from excessive
sweating, vomiting, diarrhea, burns and diuretics.
§ Result of an increase in circulating AVP and/or increased renal
sensitivity to AVP, combined with any intake of free water; a
notable exception Is hyponatremia due to low solute intake.
§ The most common cause of SIADH is hyponatremia.

27. HYPERNATREMIA
§ Hypernatremia is defined as an increase in the plasma Na + concentration
to>145mM. Considerably less common than hyponatremia
§ Hypernatremia is caused by a relative deficit of water in relation to sodium
which can result from
ØNet water loss : accounts for majority of cases
ØPure water loss
ØHypotonic fluid loss
ØHypertonic gain results from iatrogenic sodium loading

28. z
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