Human Excretion and Kidney Physiology

Glomerular filtration rate (GFR) is driven by net filtration pressure. Compression of the renal capsule increases hydrostatic pressure in the Bowman space, which opposes filtration and thus decreases GFR.

Drinking sea water increases blood osmolarity due to its high salt concentration, which strongly stimulates osmoreceptors in the hypothalamus to secrete antidiuretic hormone (ADH) to conserve water. Distilled water would lower osmolarity and decrease ADH secretion, while isotonic water causes little change.

Kidneys play a very large role in human osmoregulation by regulating the amount of water reabsorbed from glomerular filtrate in kidney tubules, which is controlled by hormones such as antidiuretic hormone(ADH), aldosterone and corticotropin. 

When the level of water in blood goes up for example in cold or when we had a lot to drink, the hypothalamus detects the change and sends a message to the pituitary. The release of ADH into the blood is slowed down or even stopped. Without ADH the kidneys will not save as much water and we produce large volumes of dilute urine. The level of water in the blood falls back to the normal level.

The reabsorption of water in the earlier parts of the nephron (regardless of a person's state of hydration), independent of ADH is termed as 'obligatory reabsorption of water', whereas the water reabsorption in the distal part of the nephron (in accordance with the body's state of hydration), under the influence of ADH, is termed as 'facultative reabsorption of water'.
In facultative reabsorption, the collecting ducts become more permeable to water due to the effect of ADH, so water is reabsorbed by osmosis. Osmosis is a passive process (the diffusion of water from an area of higher water concentration to an area of lower water concentration), no expenditure of ATP energy is required in it.
Thus water reabsorption under the influence of ADH is facultative and passive reabsorption.

The primary hormone involved in regulating water loss is the antidiuretic hormone (ADH). When the body has excess water, cells in the hypothalamus of the brain respond and send a signal to the pituitary and only a small amount of ADH is released and water is lost. When we are dehydrated these same brain cells cause more ADH to be released and water leaves the collecting duct and is returned to the blood. Thus reducing the volume of urine. Adrenocortico hormones are secreted by adrenal cortex under the influence of adrenocorticotropic hormone. The major adrenal cortex enzymes are mineralocorticoids and glucocorticoids. The mineralocorticoids act on kidney tubules and help in maintaining sodium and potassium balance.

Vasopressin also known as antidiuretic hormone (ADH), is a neurohypophysial hormone found in most mammals. Its two primary functions are to retain water in the body and to constrict blood vessels. Antidiuretic hormone binds to receptors on cells in the collecting ducts of the kidney and promotes reabsorption of water back into the circulation. In the absence of antidiuretic hormone, the collecting ducts are virtually impermeable to water, and it flows out as urine. 

When renal blood flow is reduced, juxtaglomerular cells in the kidneys convert the prorenin present in the blood into renin and secrete it directly into circulation. Plasma renin then carries out the conversion of angiotensinogen released by the liver to angiotensin I. Angiotensin I is subsequently converted to angiotensin II by the enzyme angiotensin-converting enzyme found in the lungs. Angiotensin II is a potent vasoactive peptide that causes blood vessels to constrict, resulting in increased blood pressure.

ADH targets nephrons in kidney to increase water reabsorption and thereby decreasing water content in urine. Inability of neurohypophysial system to produce ADH, causes excess urine production with resultant ion loss from blood. This condition is known as diabetes insipidus (watery urine). 

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 (Distal convoluted tubule and Collecting duct), thereby preventing diuresis. An increase in body fluid volume can switch off the osmoreceptors and suppress the ADH release to complete the feedback. ADH mainly acts on collecting ducts of kidney and increase the water reabsorption in this part.

Vasopressin (ADH) is a peptide hormone, secreted from the posterior pituitary, increases water permeability of the kidney's collecting duct and distal convoluted tubule by inducing translocation of aquaporin-CD water channels in the collecting duct plasma membrane. Thus, increases the water absorption in the collecting duct and helps in water retaintion in the body.

ADH regulates the water balance in body by decreasing the excretion of free water from kidney (antidiuretic effect). It does so by increasing the permeability of ADH responsive cells in linings of distal convoluted tubules and collecting ducts of renal nephrons. 

Anti-diuretic hormone or the vasopressin is secreted by the hypothalamus and is stored and released by the posterior pituitary. This hormone is responsible for maintaining blood volume. When salty food is consumed, it increases the ions in the bloodstream and reduces the volume of the blood. The ADH will be released in this condition, that will directly act on the water reabsorbing channels in the collecting ducts of the nephrons. So, water will be reabsorbed from the filtrate and restored back to the blood. 

ADH is secreted by pituitary gland. It increases the water permeability of distal convoluted tubules and collecting tubules, hence, plays a significant role in water re-absorption. The absence of ADH will reduce water reabsorption which may lead to water diuresis or diabetes insipidus.

Renin is an enzyme secreted by the kidneys that converts angiotensinogen into angiotensin I, which is a key step in the renin-angiotensin-aldosterone system.