Mechanism of Compensation for Dehydration

The Mechanisms In Fluid Balance

a) ADH

b) Thirst mechanism - when there is a deficit of water with decreased volume and increased osmolarity , the thirst center in the hypothalamus is stimulated which prompts the individual to ingest fluid

c) Aldosterone

d) Sympathetic nervous system - system that is responsible for fight of flight response

Action of ADH.

ADH (Antidiuretic Hormone, Arginine vasopressin; AVP; Vasopressin)
- produced in the hypothalamus and released at the posterior pituitary gland
- causes reabsorption of H2O at the distal tubule of the nephron

· losing water causes increased solute concentration in the plasma

· osmoreceptors detect the increased concentration of solutes in the interstitial fluid, which reflects the increase osmolarity in the plasma

· ADH is released into the plasma at the posterior pituitary

· ADH acts on the distal convulated tube and the collecting duct. It promotes the addition of water channels and therefore increases the permeability of the DCT and CD to water.

· More water reabsorbed into the plasma, less urine produced. Plasma osmolarity decreases again

Thirst Mechanism.

· Primary regulator of water intake and involves hormonal and neural input as well as voluntary behavior.

· Plasma osmotic pressure (plasma osmolarity) increases stimulating the osmoreceptors in the thirst centre of the hypothalamus .

· Decrease blood volume and pressure causes release of rennin and the production of angiotensin II which stimulates the thirst centre.

· Salivation is reduced as the mouth and throat feel dry. A sense of thirst is formed.


The Renin-Angiotensin-Aldosterone system.

· When someone suffers from hypovolemia, there is blood volume lost as well as a drop in blood pressure.

· Decrease in pressure in the afferent arteriole is sensed by the baroreceptors which leads to the stimulation of the release of renin from the juxtaglomerular cells of the afferent arteriole.

· Renin converts a protein into angiotensin (I) as an Angiotensin-converting-enzyme (ACE) converts angiotensin(I) to angiotensin (II).

· Angiotensin II reduces urine production by two ways:

a) It leads to vasoconstriction of the afferent and efferent arterioles increasing renal vascular resistance and reducing renal blood flow. This causes a decrease in the glomerular capillary hydrostatic pressure and the glomerular filtration rate (GFR). Reduction of GFR will result to reduction in urine production.

b) Secondary role in volume regulation by stimulating the synthesis of aldosterone from the adrenal gland.

Aldosterone in turn leads to increase of pemearbility of the DCT and CD to Na+and Cl-. More Na+and Cl- absorbed into the blood plasma which eventually followed by the flow of water into the blood plasma. Hence volume of urine is reduced.

Sympathetic Nervous System.

· Volume depletion will lead to decreased blood volume and venous return to the heart.

· This is then sensed by the baroreceptors (volume receptors) at the atria and pulmonary veins and pressure receptors at the renal afferent arteriole which will lead to the sympathetic activity.

· This will result in sympathetically mediated vasoconstriction. (sim