The functioning of the kidneys is efficiently monitored and regulated by
hormonal feedback mechanisms involving the hypothalamus, JGA and
to a certain extent, the heart.
Osmoreceptors in the body are activated by changes in blood volume,
body fluid volume and ionic concentration. An excessive loss of fluid from
the body can activate these receptors which stimulate the hypothalamus
to release antidiuretic hormone (ADH) or vasopressin from the
neurohypophysis. ADH facilitates water reabsorption from latter parts of
the tubule, thereby preventing diuresis. An increase in body fluid volume
can switch off the osmoreceptors and suppress the ADH release to complete
the feedback. ADH can also affect the kidney function by its constrictory
effects on blood vessels. This causes an increase in blood pressure. An
increase in blood pressure can increase the glomerular blood flow and
thereby the GFR.
The JGA plays a complex regulatory role. A fall in glomerular blood
flow/glomerular blood pressure/GFR can activate the JG cells to release
renin which converts angiotensinogen in blood to angiotensin I and
further to angiotensin II. Angiotensin II, being a powerful
vasoconstrictor, increases the glomerular blood pressure and thereby
GFR. Angiotensin II also activates the adrenal cortex to release
Aldosterone. Aldosterone causes reabsorption of Na+ and water from
the distal parts of the tubule. This also leads to an increase in blood
pressure and GFR. This complex mechanism is generally known as
the ReninAngiotensin mechanism.
An increase in blood flow to the atria of the heart can cause the release
of Atrial Natriuretic Factor (ANF). ANF can cause vasodilation (dilation of
blood vessels) and thereby decrease the blood pressure. ANF mechanism,
therefore, acts as a check on the reninangiotensin mechanism.