
Role of the Kidney in Long-Term Regulation of Arterial Pressure and in Hypertension: The Integrated System for Pressure Control.
Renal–Body Fluid System for Arterial Pressure Control
The renal–body fluid system for arterial pressure control is a simple one: When the body contains too much extracellular fluid, the blood volume and arterial pressure rise. The rising pressure in turn has a direct effect to cause the kidneys to excrete the excess extracellular fluid, thus returning the pressure back toward normal.
In the phylogenetic history of animal development, this renal–body fluid system for pressure control is a primitive one. It is fully operative in one of the lowest of vertebrates, the hagfish. This animal has a low arterial pressure, only 8 to 14 mm Hg, and this pressure increases almost directly in proportion to its blood volume. The hagfish continually drinks sea water, which is absorbed into its blood, increasing the blood volume as well as the pressure. However, when the pressure rises too high, the kidney simply excretes the excess volume into the urine and relieves the pressure. At low pressure, the kidney excretes far less fluid than is ingested. Therefore, because the hagfish continues to drink, extracellular fluid volume, blood volume, and pressure all build up again to the higher levels.
Throughout the ages, this primitive mechanism of pressure control has survived almost exactly as it functions in the hagfish; in the human being, kidney output of water and salt is just as sensitive to pressure changes as in the hagfish, if not more so. Indeed, an increase in arterial pressure in the human of only a few millimeters of mercury can double renal output of water, which is called pressure diuresis, as well as double the output of salt, which is called pressure natriuresis. In the human being, the renal–body fluid system for arterial pressure control, just as in the hagfish, is the fundamental basis for long-term arterial pressure control. However, through the stages of evolution, multiple refinements have been added to make this system much more exact in its control in the human being. An especially important refinement, as we shall see, has been addition of the renin-angiotensin mechanism.
Experimental studies have shown that an increase in salt intake is far more likely to elevate the arterial pressure than is an increase in water intake. The reason for this is that pure water is normally excreted by the kidneys almost as rapidly as it is ingested, but salt is not excreted so easily. As salt accumulates in the body, it also indirectly increases the extracellular fluid volume for two basic reasons:
When there is excess salt in the extracellular fluid, the osmolality of the fluid increases, and this in turn stimulates the thirst center in the brain, making the person drink extra amounts of water to return the extracellular salt concentration to normal. This increases the extracellular fluid volume.
The increase in osmolality caused by the excess salt in the extracellular fluid also stimulates the hypothalamic-posterior pituitary gland secretory mechanism to secrete increased quantities of antidiuretic hormone. The antidiuretic hormone then causes the kidneys to reabsorb greatly increased quantities of water from the renal tubular fluid, thereby diminishing the excreted volume of urine but increasing the extracellular fluid volume.
Thus, for these important reasons, the amount of salt that accumulates in the body is the main determinant of the extracellular fluid volume. Because only small increases in extracellular fluid and blood volume can often increase the arterial pressure greatly, accumulation of even a small amount of extra salt in the body can lead to considerable elevation of arterial pressure.
Regulation of Extracellular Fluid Osmolarity and Sodium Concentration
For the cells of the body to function properly, they must be bathed in extracellular fluid with a relatively constant concentration of electrolytes and other solutes. The total concentration of solutes in the extracellular fluid—and therefore the osmolarity—is determined by the amount of solute divided by the volume of the extracellular fluid. Thus, to a large extent, extracellular fluid sodium concentration and osmolarity are regulated by the amount of extracellular water. The body water in turn is controlled by (1) fluid intake, which is regulated by factors that determine thirst, and (2) renal excretion of water, which is controlled by multiple factors that influence glomerular filtration and tubular reabsorption.
The Kidneys Excrete Excess Water by Forming a Dilute Urine
The normal kidney has tremendous capability to vary the relative proportions of solutes and water in the urine in response to various challenges. When there is excess water in the body and body fluid osmolarity is reduced, the kidney can excrete urine with an osmolarity as low as 50 mOsm/L, a concentration that is only about one sixth the osmolarity of normal extracellular fluid. Conversely, when there is a deficit of water and extracellular fluid osmolarity is high, the kidney can excrete urine with a concentration of 1200 to 1400 mOsm/L. Equally important, the kidney can excrete a large volume of dilute urine or a small volume of concentrated urine without major changes in rates of excretion of solutes such as sodium and potassium. This ability to regulate water excretion independently of solute excretion is necessary for survival, especially when fluid intake is limited.
Antidiuretic Hormone Controls Urine Concentration
There is a powerful feedback system for regulating plasma osmolarity and sodium concentration that operates by altering renal excretion of water independently of the rate of solute excretion. A primary effector of this feedback is antidiuretic hormone (ADH), also called vasopressin.
When osmolarity of the body fluids increases above normal (that is, the solutes in the body fluids become too concentrated), the posterior pituitary gland secretes more ADH, which increases the permeability of the distal tubules and collecting ducts to water.This allows large amounts of water to be reabsorbed and decreases urine volume but does not markedly alter the rate of renal excretion of the solutes.
When there is excess water in the body and extracellular fluid osmolarity is reduced, the secretion of ADH by the posterior pituitary decreases, thereby reducing the permeability of the distal tubule and collecting ducts to water, which causes large amounts of dilute urine to be excreted. Thus, the rate of ADH secretion determines, to a large extent, whether the kidney excretes a dilute or a concentrated urine.
Your Kidneys Conserve the Water within your body by excreting a concentrated urine
The ability of the kidney to form a urine that is more concentrated than plasma is essential for survival of mammals that live on land, including humans. Water is continuously lost from the body through various routes, including the lungs by evaporation into the expired air, the gastrointestinal tract by way of the feces, the skin through evaporation and perspiration, and the kidneys through the excretion of urine. Fluid intake is required to match this loss, but the ability of the kidney to form a small volume of concentrated urine minimizes the intake of fluid required to maintain homeostasis, a function that is especially important when water is in short supply.
When there is a water deficit in the body, the kidney forms a concentrated urine by continuing to excrete solutes while increasing water reabsorption and decreasing the volume of urine formed. The human kidney can produce a maximal urine concentration of 1200 to 1400 mOsm/L, four to five times the osmolarity of plasma. Some desert animals, such as the Australian hopping mouse, can concentrate urine to as high as 10,000 mOsm/L. This allows the mouse to survive in the desert without drinking water; sufficient water can be obtained through the food ingested and water produced in the body by metabolism of the food. Hence fruit & vegetables being the best thing to ingest in order to hydrate the human body sufficiently. Animals adapted to aquatic environments, such as the beaver, have minimal urine concentrating ability; they can concentrate the urine to only about 500 mOsm/L.
Obligatory Urine Volume
The maximal concentrating ability of the kidney dictates how much urine volume must be excreted each day to rid the body of waste products of metabolism and ions that are ingested. A normal 70-kilogram human must excrete about 600 milliosmoles of solute each day. If maximal urine concentrating ability is 1200 mOsm/L, the minimal volume of urine that must be excreted, called the obligatory urine volume, can be calculated as
This minimal loss of volume in the urine contributes to dehydration, along with water loss from the skin, respiratory tract, and gastrointestinal tract, when water is not available to drink.
The limited ability of the human kidney to concentrate the urine to a maximal concentration of 1200 mOsm/L explains why severe dehydration occurs if one attempts to drink seawater. Sodium chloride concentration in the oceans averages about 3.0 to 3.5 per cent, with an osmolarity between about 1000 and 1200 mOsm/L. Drinking 1 liter of seawater with a concentration of 1200 mOsm/L would provide a total sodium chloride intake of 1200 milliosmoles. If maximal urine concentrating ability is 1200 mOsm/L, the amount of urine volume needed to excrete 1200 milliosmoles would be 1200 milliosmoles divided by 1200 mOsm/L, or 1.0 liter. Why then does drinking seawater cause dehydration? The answer is that the kidney must also excrete other solutes, especially urea, which contribute about 600 mOsm/L when the urine is maximally concentrated. Therefore, the maximum concentration of sodium chloride that can be excreted by the kidneys is about 600 mOsm/L. Thus, for every liter of seawater drunk, 2 liters of urine volume would be required to rid the body of 1200 milliosmoles of sodium chloride ingested in addition to other solutes such as urea. This would result in a net fluid loss of 1 liter for every liter of seawater drunk, explaining the rapid dehydration that occurs in shipwreck victims who drink seawater. However, a shipwreck victim’s pet Australian hopping mouse could drink with impunity all the seawater it wanted.
