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 Renin-Angiotensin 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 renin-angiotensin mechanism.