Regulation of the Kidneys
While it is true that your kidneys can excrete a hyperosmotic urine, it is not always desirable to do so. Nevertheless, if you are dehydrated and water is unavailable, the kidneys can excrete a small volume of hyperosmotic urine as concentrated as 1200 mosm/ L, making it possible to discharge wastes with a minimal water loss.
But if you have consumed an excessive amount of fluid, the kidneys can actually excrete a large volume of hypoosmotic urine as dilute as 70 mosm/L, making it possible to eliminate a lot of water without losing essential salts. The kidney is a versatile osmoregulatory organ, where water and salt reabsorption are subject to a combination of nervous and hormonal controls. (Hormones, chemical signals between various organs of the body, are discussed in detail in the next chapter. Here, we are concerned only with the effects of a few hormones on the kidneys.)
One hormone important in osmoregulation is anti-diuretic hormone, or ADH. It is produced in a part of the brain called the hypothalamus and then stored and released from an organ called the pituitary gland, which is positioned just below the hypothalamus. Osmoreceptor cells located in the hypothalamus monitor the osmolarity of blood, triggering the release of ADH when an increase in the blood osmolarity is detected.
The hormone is discharged into the bloodstream and reaches the kidney. The main targets of ADH are the distal convoluted tubules and the collecting ducts of the kidney, where the hormone increases the permeability of the epithelium to water. This amplifies water reabsorption, which reduces the osmolarity of the blood.
By negative feedback, the subsiding osmolarity of the blood reduces the activity of osmoreceptor cells in the hypothalamus, and less ADH is secreted. When very little ADH is released, as would occur after consumption of a large volume of water has lowered the blood osmolarity, then the kidneys would absorb little water, resulting in copious excretion of dilute urine. (Voluminous urination is called diuresis, and it is because ADH opposes this state that it is called antidiuretic hormone.) Alcohol can perturb water balance by inhibiting the release of ADH, causing excessive loss of water in the urine and dehydrating the body-perhaps some of the symptoms of a hangover are due to this dehydration. Normally, however, blood osmolarity, ADH release, and water reabsorption in the kidney are all linked in a feedback loop that contributes to homeostasis.
A second system regulating kidney function involves a specialized tissue called the juxtaglomerular apparatus (JGA), located in the vicinity of the afferent arteriole that supplies blood to the glomerulus (Figure 40.14b). When the blood pressure in the afferent arteriole drops, or when the Na + concentration of the blood is too low, the JGA releases an enzyme called renin to the bloodstream. Within the blood, renin activates a plasma protein called angiotensin. The active form of this orotein, called angiotensin II, functions as a hormone, with multiple effects that increase the Na+ concentration of the blood and raise blood pressure. For example, angiotensin II causes a generalized constriction of arterioles, which raises blood pressure.
Increasing pressure within the afferent arterioles of the nephrons, in turn, increases filtration rate. Angiotensin II also acts remotely on the kidney by stimulating the adrenal glands, organs located on top of the kidneys, to release another hormone called aldoste-rone. This hormone acts on the distal convoluted tubules of the nephrons, stimulating the reabsorption of Na + . Because water follows the Na+ out of the renal tubule by osmosis, aldosterone also increases blood volume and blood pressure. It was a drop in blood pressure or a deficiency of Na+ that triggered renin release from the JGA in the first place, and the various responses increase blood pressure and Na+ concentration, thus reducing the release of renin-another example of a feedback circuit functioning in homeostasis.
It may seem that the functions of ADH and aldosterone are redundant, but this is not the case. It is true that both hormones increase water reabsorption, but they are enlisted to counter different osmoregulatory problems. The release of ADH is a response to an increase in the osmolarity of the blood, as occurs when the body is dehydrated-by inadequate intake of water, for instance. But imagine a situation that causes an excessive loss of salt and body fluids-an injury, for example, or severe diarrhea. This reduces the blood's volume without increasing its osmolarity. Aldosterone would save the day by increasing water and a Na+ reabsorption in response to the drop in blood volume caused by fluid loss. Normally, ADH and aldosterone are partners in homeostasis; ADH alone would lower blood Na + concentration by stimulating water reabsorption in the kidney, but aldosterone helps maintain balance by stimulating Na+ reabsorption.
Still another hormone, atrial natriuretic protein (ANP), opposes the renin-angiotensin-aldosterone system. The wall of the atrium of the heart releases ANP in response to an increase in blood volume and pressure, and the hormone counters by inhibiting the release of renin from the juxtaglomerular apparatus and also directly reducing aldosterone release from the adrenal glands. These actions decrease Na+ reabsorption and lower blood volume and pressure. Thus, ADH, the renin-angiotensin-aldosterone trio, and ANP provide an elaborate system of checks and balances that regulate the kidney's ability to control the osmolarity, salt concentration, volume, and pressure of blood.
Having considered the mammalian kidney and its regulation in detail, we can now compare the structures and functions of kidneys in other vertebrate classes.