Page 114 - Textbook of Pathology, 6th Edition
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SECTION I
General Pathology and Basic Techniques
Figure 5.4 Mechanisms involved in oedema by sodium and water retention.
sinus and aortic arch which, in turn, send the sympathetic ADH mechanism. Retention of sodium leads to retention
outflow via the vasomotor centre in the brain. As a result of of water secondarily under the influence of anti-diuretic
this, renal ischaemia occurs which causes reduction in the hormone (ADH) or vasopressin. This hormone is secreted
glomerular filtration rate, decreased excretion of sodium in by the cells of the supraoptic and paraventricular nuclei in
the urine and consequent retention of sodium. the hypothalamus and is stored in the neurohypophysis
Extra-renal mechanism involves the secretion of (posterior pituitary). The release of hormone is stimulated
aldosterone, a sodium retaining hormone, by the renin- by increased concentration of sodium in the plasma and
angiotensin-aldosterone system. Renin is an enzyme secreted hypovolaemia. Large amounts of ADH produce highly
by the granular cells in the juxta-glomerular apparatus. Its concentrated urine.
release is stimulated in response to low concentration of The possible factors responsible for causation of oedema
sodium in the tubules. Its main action is stimulation of the by excessive retention of sodium and water in the
angiotensinogen which is α -globulin or renin substrate extravascular compartment via stimulation of intrinsic renal
2
present in the plasma. On stimulation, angiotensin I, a and extra-renal mechanisms as well as via release of ADH
decapeptide, is formed in the plasma which is subsequently are as under:
converted into angiotensin II, an octapeptide, in the lungs i) Reduced glomerular filtration rate in response to
and kidneys by angiotension converting enzyme (ACE). hypovolaemia.
Angiotensin II stimulates the adrenal cortex to secrete aldo- ii) Enhanced tubular reabsorption of sodium and
sterone hormone. Aldosterone increases sodium reabsorption consequently its decreased renal excretion.
in the renal tubules and sometimes causes a rise in the blood iii) Increased filtration factor i.e. increased filtration of plasma
pressure. from the glomerulus.

