The extracellular volume is controlled by the total body
content of sodium because Na+ is by far the most abundant active
solutes in ECF. Control of body’s Na+ is excreted by tight control
over renal excretion, that is achieved by activation of receptors which
responds to extracellular volume rather than the change in sodium
concentration. Thus the defenses of ECF volume are
·
Extrarenal volume receptors mechanism
o Vasopressin
(ADH) mechanism
o Atrial
natriuretic peptide mechanism
·
Intrarenal mechanism
o Rennin-angiotensin-aldosterone
mechanism
Volume receptor mechanism:
A slight
reduction in effective circulatory volume inhibits volume receptors in the
atria, aortic arch sinus body and major thoracic veins. This results in..
·
Increased sympathetic nerve activity and a rise in
catecholamines.
·
Increased vasopressin secretion (ADH)
Both this response cause antidiuresis and thus increase
circulatory volume. Conversely an increase in ECF volume causes opposite
effect.
·
Decrease in ADH secretion – diuresis
·
Increase in ANP secretion – natriuresis, diuresis.
Intrarenal mechanism:
Receptors in the walls of the glomerular afferent arterioles
respond via the juxtaglomerular apparatus to changes in renal perfusion and
control the activity of the renin-angiotesin-aldosterone system. A decrease in
effective ECF volume leads to decrease in renal perfusion and stimulates renin
release that in turns increase circulatory angiotensin-II. Angiotensin-II
causes
·
Vasoconstriction
·
Aldosterone secretion: Na+ and H2O
retention.
·
Thirst mechanism: drinking
·
Vasopressin secretion: antidiuresis
The
final common pathway for all the regulatory systems discussed is to increase or
decrease the renal excretion of Na+ in the event of an increase or
decrease in effective ECF volume. An increase in the reabsorbtion of Na+
with concomitant retention of H2O expands the vascular and
interstitial compartments while increase Na+ excretion has the
opposite effect.
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