General physiology
Regulation of ECF
By Assist. Prof. Dr. Majida Alqayim
Departement of physiology and pharmacology
College of veterinary medicine
University of Baghdad
Physiology of body fluids
Body Fluids Compartments:
•
•
•
Water comprised about 70% of the weight of most vertebrates, is
distributed in the :1-intracellular(ICF): fluid inside the cells. 2/3 volume of fluids in body(15%
of body weight)
2- extracellular (plasma and interstitial) (ECF): fluid outside the cells.1/3
volume of fluids in body(40% of body weight)
3- transcellular (alimentary tract, urine, synovial fluid) (5% of body weight)
The electrolyte concentrations , pH, and the osmolality of intracellular and
extracellular fluids must be regulated . The process of regulating the
concentration
of water and mineral salts in the body fluid is called
:
osmoregulation, the animal cell has always to be surrounded by an isotonic
solution. Osmoregulation of the extracellular fluid is achieved by regulated
addition and subtraction of free water from the extracellular fluid, thus diluting
or concentrating the already present electrolytes. via adding or removing free
water from the ECF.
According to the differences of solutes concentration , extracellular
solutions will be differ in their osmolality and classify in to 3
types
Isotonic- Means having the same concentration of solutes so it will
not affect the cell.
Hypotonic- Means a solution with low solute concentration, so
when a cell is placed in a hypotonic solution, it takes up water
and swells and may burst.
Hypertonic- Means a solution with more concentration, i.e more
solutes. For example, if a cell is placed in a hypertonic solution, it
will shrink in size as water moves from hypertonic to hypotonic.
Regulation of fluid concentration
• These processes are regulated by means of negative
feedback mechanism control circuits which sense the
extracellular fluid osmolite concentration and then
coordinate free water addition and subtraction in an effort
to maintain relatively stable values of osmolite
concentration. When ECF osmolity rises excessively, these
mechanisms promote addition of free water to the ECF,
thus reducing ECF osmolite. In contrast, when ECF osmolite
concentration drops excessively, these processes enhance
water loss from the extracellular fluid, thus returning ECF
osmolite to its set point. This organization is work in a reflex
behavior.
• This reflex is include a coordination between the central
and peripheral receptors , central controller in the
hypothalamus and the effective organs which are mainly
kidney and blood vessels
 Central receptors
There are receptors and other systems in the body that detect a decreased volume or an
increased osmolite concentration. They signal to the central nervous system, where central
processing succeeds. Some sources,therefore, distinguish "extracellular thirst" from
"intracellular thirst", where extracellular thirst is thirst generated by decreased volume and
intracellular thirst is thirst generated by increased osmolite concentration
Hypothalmic centers:Clusters of cells (osmoreceptors) in the organum vasculosum of the lamina
terminalis (OVLT) and subfornical organ (SFO), which lie outside of the blood brain barrier can
detect the concentration of blood plasma and the presence of angiotensin II in the
blood.
 Peripheral receptors:
 Cardiopulmonary baroreceptors: Baroreceptors alert the brain of increases in
blood volume (hence increased blood pressure)
Sympathetic nervous system impulses to the kidney
 Juxtaglomerular cells (intra renal baroreceptors) and the macula densa: The
renin-angiotensin mechanism triggers the release of aldosterone. This is
mediated by juxtaglomerular apparatus, which releases renin in response to:
 Sympathetic nervous system stimulation
 Decreased filtrate osmolality
 Decreased stretch due to decreased blood pressure
 Atrial Stretch receotors
Central Controller
Central Controller are two types:
Hypothalmic Volumetric thirst: Stimulated by Decreased volume
The loss of blood volume is detected by cells in the kidneys and triggers
thirst for both water and salt via the renin-angiotensin system.
Feedback signals that inhibit the thirst centers include:
Moistening of the mucosa of the mouth and throat
Activation of stomach and intestinal stretch receptors
Hypothalamic Osmometric thirst: Stimulated by Cellular
dehydration and osmoreceptor . Stimulation trigger or inhibit
ADH release Vasopressin (arginine vasopressin, AVP;
antidiuretic hormone, ADH) is a peptide hormone formed in
the hypothalamus, then transported via axons to, and released
from, the posterior pituitary into the blood.
Mechanism for regulation of ECF:
1- Release of ADH(AVP)
The primary function of AVP in the body is to regulate extracellular fluid volume.
factors influence on AVP release
There are several mechanisms regulating the release of AVP, the most important of which are the
following:
1- Hypovolemia, as occurs during hemorrhage and dehydration, results in a decrease in atrial
pressure. Specialized stretch receptors within the atrial walls and large veins
(cardiopulmonary baroreceptors) entering the atria decrease their firing rate when there is a
fall in atrial pressure. Afferent nerve fibers from these receptors synapse within the nucleus
tractus solitarius of the medulla, which sends fibers to the hypothalamus, a region of the
brain that controls AVP release by the pituitary. Atrial receptor firing normally inhibits the
release of AVP by the posterior pituitary. AVP has two principle sites of action: the kidney and
blood vessels. With hypovolemia or decreased central venous pressure, the decreased firing
of atrial stretch receptors leads to an increase in AVP release.
2- Hypotension, which decreases arterial baroreceptor firing, leads to enhanced sympathetic
activity that increases AVP release.
Hypothalamic osmoreceptors sense extracellular osmolarity and stimulate AVP release when
osmolarity rises, as occurs with dehydration.
3- Angiotensin II receptors located in a region of the hypothalamus regulate AVP release – an
increase in angiotensin II simulates AVP release.
Factors that specifically trigger ADH release include prolonged fever; excessive sweating,
vomiting, or diarrhea; severe blood loss; and traumatic burns. ADH promote water
reabsorption in collecting ducts . Low ADH levels produce dilute urine and reduced volume of
body fluids. High ADH levels produce concentrated urine.
Mechanism for regulation of ECF:
1- Release of ADH(AVP)
Mechanism for regulation of ECF:
2- Renin- angiotensin system
Renin- angiotensin system is a hormone system that regulates blood pressure and fluid
balance The system can be activated by different mechanism:
1- when there is a loss of blood volume or a drop in blood pressure (such as
in hemorrhage or dehydration). This loss of pressure is interpreted by baroreceptors in the carotid
sinus.
2- a decrease in the filtrate NaCl concentration and/or decreased filtrate flow rate will stimulate
the macula densa to signal the juxtaglomerular cells to release renin.
3- If the perfusion of the juxtaglomerular apparatus in the kidney's macula densa decreases, then the
juxtaglomerular cells (granular cells, modified pericytes in the glomerular capillary) release
the enzyme renin.
Renin cleaves a zymogen, an inactive peptide, called angiotensinogen, converting it into angiotensin I.
Angiotensin I is then converted to angiotensin II by angiotensin-converting enzyme (ACE), which is
thought to be found mainly in lung capillaries.
Angiotensin II is the major bioactive product of the renin-angiotensin systemwhich prompts :-
1-Vassoconstriction
2-Release of aldosterone
3- ADH
Mechanism for regulation of ECF:
2- Renin- angiotensin system
Mechanism for regulation of ECF:
3- Role of Aldosterone
Aldosterone, is the steroid hormone produced in the zona
glomerulosa of the adrenal cortex. Aldosterone works in
the cells of the cortical collecting duct. Aldosterone saves
salt. It works to increase Na+reabsorption by promoting
the expression of all the channels and pumps related to
Na+ it is the principal regulator of Na+ reabsorption
Aldosterone brings about its effects (diminished urine
output and increased blood volume) .
Aldosterone is responsible for the reabsorption of about
2% of filtered sodium in the kidneys, which is nearly
equal to the entire sodium content in human blood
under normal glomerular filtration rates.
Mechanism for regulation of ECF:
3- Role of Aldosterone
Mechanisms for regulation of ECF:
4- Atrial Stretch receotors
• Atrial Natriuretic Peptide (ANP)
• An additional mechanism involved in the regulation of
Na+ levels involves the hormone atrial natriuretic
peptide (ANP). This hormone is synthesized by cells in
the atrium of the heart, and is released in response to
distension of the atria, in other words, when plasma
volume increases. The effect of ANP is to
increase natriuresis, that is the excretion of Na+ in the
urine. ANP increases natriuresis by increasing GFR and
decreasing Na+ reabsorption. ANP works to oppose the
effects of the renin-angiotensin-aldosterone system,
preventing plasma overload by preventing excessive
Na+ levels in the body
Mechanisms for regulation of ECF
5-Influence of Other Hormones on Sodium Balance
– Estrogens:
• Enhance NaCl reabsorption by renal tubules
• May cause water retention during menstrual cycles
• Are responsible for edema during pregnancy
– Progesterone:
• Decreases sodium reabsorption
• Acts as a diuretic, promoting sodium and water loss
– Glucocorticoids - enhance reabsorption of sodium
and promote edema