How is the composition of urine regulated?

The composition of urine depends upon food and fluid consumed by an individual. There are two ways in which it the composition is regulated. 

They are as follows: 

1. Regulating water reabsorption through ADH 

2. Electrolyte reabsorption though RAAS 

3. Atrial Natriuretic Peptide

i) Regulating water reabsorption through ADH: 

Hypothalamus in the midbrain has special receptors called osmoreceptors which can detect change in osmolarity (measure of total number of dissolved particles per liter of solution) of blood. 

If osmolarity of blood increases due to water loss from the body (after eating namkeen or due to sweating), osmoreceptors trigger release of Antidiuretic hormone (ADH) from neurohypophysis (posterior pituitary). ADH stimulates reabsorption of water from last part of DCT and entire collecting duct by increasing the permeability of cells. 

This leads to reduction in urine volume and decrease in osmolarity of blood. 

Once the osmolarity of blood comes to normal, activity of osmoreceptor cells decreases leading to decrease in ADH secretion. This is called negative feedback.

In case of hemorrhage or severe dehydration too, osmoreceptors stimulate ADH secretion. ADH is important in regulating water balance through kidneys. 

In absence of ADH, diuresis (dilution of urine) takes place and person tends to excrete large amount of dilute urine. This condition called as diabetes insipidus. 

[Note: Hypothalamus is a part of forebrain] 

ii) Electrolyte reabsorption through RAAS: 

Another regulatory mechanism is RAAS (Renin Angiotensin Aldosterone System) by Juxta Glomerular Apparatus (JGA).

Whenever blood supply (due to change in blood pressure or blood volume) to afferent arteriole decreases (e.g. low BP/dehydration), JGA cells release Renin. Renin converts angiotensinogen secreted by hepatocytes in liver to Angiotensin I. ‘Angiotensin converting enzyme’ further modifies Angiotensin I to Angiotensin II, the active form of hormone. It stimulates adrenal cortex to release another hormone called aldosterone that stimulates DCT and collecting ducts to reabsorb more Na and water, thereby increasing blood volume and pressure. 

iii) Atrial natriuretic peptide (ANP): 

A large increase in blood volume and pressure stimulates atrial wall to produce atrial natriuretic peptide (ANP). ANP inhibits Na+ and Cl reabsorption from collecting ducts inhibits release of renin, reduces aldosterone and ADH release too. This leads to a condition called Natriuresis (increased excretion of Na+ in urine) and diuresis.