Question

You go for a long run on an extremely hot, humid day, and as such, you sweat way more than you typically would. Describe what is occurring to the water balance in your body, including:

a. An overview of the differences between the intracellular fluid and the extracellular fluid compartments

b. Movement of water/fluids between the compartments

c. The role of sodium in water balance, how it is regulated, and how sodium contributes to the body’s homeostatic equilibrium

d. Your body’s response to the disruption in water balance and how it is compensated for

Answer 1

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Intracellular fluid Intracellular fluid is a fluid inside the cell membrane, containing dissolved ions and other components Found inside the cell Comprises the cytosol The concentration of sodium ions is low and the concentration of potassium ions is high Comprises 55% of body water Comprises 33% of total body weight Comprises 19 L of total body fluids

Extracelluar fluid Extracellular fluid is the fluid found outside of the cell, aiding the functioning of a particular tissue Found outside the cell Comprises plasma, tissue fluid, and transcellular fluid The concentration of sodium ions is high and the concentration of potassium ions is low Comprises about 45% of body water Comprises 27% of total body weight Comprises 23 L of total body fluids

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Hydrostatic pressure, the force exerted by a fluid against a wall, causes movement of fluid between compartments. The hydrostatic pressure of blood is the pressure exerted by blood against the walls of the blood vessels by the pumping action of the heart. In capillaries, hydrostatic pressure (also known as capillary blood pressure) is higher than the opposing “colloid osmotic pressure” in blood—a “constant” pressure primarily produced by circulating albumin—at the arteriolar end of the capillary .This pressure forces plasma and nutrients out of the capillaries and into surrounding tissues. Fluid and the cellular wastes in the tissues enter the capillaries at the venule end, where the hydrostatic pressure is less than the osmotic pressure in the vessel. Filtration pressure squeezes fluid from the plasma in the blood to the IF surrounding the tissue cells. The surplus fluid in the interstitial space that is not returned directly back to the capillaries is drained from tissues by the lymphatic system, and then re-enters the vascular system at the subclavian veins.Net filtration occurs near the arterial end of the capillary since capillary hydrostatic pressure (CHP) is greater than blood colloidal osmotic pressure (BCOP). There is no net movement of fluid near the midpoint of the capillary since CHP = BCOP. Net reabsorption occurs near the venous end of the capillary since BCOP is greater than CHP

.Hydrostatic pressure is especially important in governing the movement of water in the nephrons of the kidneys to ensure proper filtering of the blood to form urine. As hydrostatic pressure in the kidneys increases, the amount of water leaving the capillaries also increases, and more urine filtrate is formed. If hydrostatic pressure in the kidneys drops too low, as can happen in dehydration, the functions of the kidneys will be impaired, and less nitrogenous wastes will be removed from the bloodstream. Extreme dehydration can result in kidney failure.

Fluid also moves between compartments along an osmotic gradient. Recall that an osmotic gradient is produced by the difference in concentration of all solutes on either side of a semi-permeable membrane. The magnitude of the osmotic gradient is proportional to the difference in the concentration of solutes on one side of the cell membrane to that on the other side. Water will move by osmosis from the side where its concentration is high (and the concentration of solute is low) to the side of the membrane where its concentration is low (and the concentration of solute is high). In the body, water moves by osmosis from plasma to the IF (and the reverse) and from the IF to the ICF (and the reverse). In the body, water moves constantly into and out of fluid compartments as conditions change in different parts of the body.

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The total amount of sodium in the body affects the amount of fluid in blood (blood volume) and around cells. The body continually monitors blood volume and sodium concentration. When either becomes too high, sensors in the heart, blood vessels, and kidneys detect the increases and stimulate the kidneys to increase sodium excretion, thus returning blood volume to normal.

When blood volume or sodium concentration becomes too low, the sensors trigger mechanisms to increase blood volume. These mechanisms include the following:

The kidneys stimulate the adrenal glands to secrete the hormone aldosterone. Aldosterone causes the kidneys to retain sodium and to excrete potassium. When sodium is retained, less urine is produced, eventually causing blood volume to increase.
The pituitary gland secretes vasopressin (sometimes called antidiuretic hormone). Vasopressin causes the kidneys to conserve water.

n addition to regulating total volume, the osmolarity (the amount of solute per unit volume) of bodily fluids is also tightly regulated. Extreme variation in osmolarity causes cells to shrink or swell, damaging or destroying cellular structure and disrupting normal cellular function.

Regulation of osmolarity is achieved by balancing the intake and excretion of sodium with that of water. (Sodium is by far the major solute in extracellular fluids, so it effectively determines the osmolarity of extracellular fluids.)

An important concept is that regulation of osmolarity must be integrated with regulation of volume, because changes in water volume alone have diluting or concentrating effects on the bodily fluids. For example, when you become dehydrated you lose proportionately more water than solute (sodium), so the osmolarity of your bodily fluids increases. In this situation the body must conserve water but not sodium, thus stemming the rise in osmolarity. If you lose a large amount of blood from trauma or surgery, however, your loses of sodium and water are proportionate to the composition of bodily fluids. In this situation the body should conserve both water and sodium.

As noted above, ADH plays a role in lowering osmolarity (reducing sodium concentration) by increasing water reabsorption in the kidneys, thus helping to dilute bodily fluids. To prevent osmolarity from decreasing below normal, the kidneys also have a regulated mechanism for reabsorbing sodium in the distal nephron. This mechanism is controlled by aldosterone, a steroid hormone produced by the adrenal cortex. Aldosterone secretion is controlled two ways:

1.The adrenal cortex directly senses plasma osmolarity. When the osmolarity increases above normal, aldosterone secretion is inhibited. The lack of aldosterone causes less sodium to be reabsorbed in the distal tubule. Remember that in this setting ADH secretion will increase to conserve water, thus complementing the effect of low aldosterone levels to decrease the osmolarity of bodily fluids. The net effect on urine excretion is a decrease in the amount of urine excreted, with an increase in the osmolarity of the urine.

2. The kidneys sense low blood pressure (which results in lower filtration rates and lower flow through the tubule). This triggers a complex response to raise blood pressure and conserve volume. Specialized cells (juxtaglomerular cells) in the afferent and efferent arterioles produce renin, a peptide hormone that initiates a hormonal cascade that ultimately produces angiotensin II. Angiotensin II stimulates the adrenal cortex to produce aldosterone.

*Note that in this setting, where the body is attempting to conserve volume, ADH secretion is also stimulated and water reabsorption increases. Because aldosterone is also acting to increase sodium reabsorption, the net effect is retention of fluid that is roughly the same osmolarity as bodily fluids

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Regulation of Water Intake

Thirst is a sensation created by the hypothalamus that drives organisms to ingest water.
Increased osmolarity in the blood acts on osmoreceptors that either stimulate the hypothalamus directly or cause the release of angiotensin II to stimulate the hypothalamus to cause thirst.
The renin –angiotensin system increases thirst as a way to increase blood volume. It is activated by high plasma osmolarity, low blood volume, low blood pressure, and stimulation of the sympathetic nervous system.

Hypothalamus-Mediated Thirst
An osmoreceptor is a sensory receptor that detects changes in osmotic pressure and is primarily found in the hypothalamus of most homeothermic organisms. Osmoreceptors detect changes in plasma osmolarity (that is, the concentration of solutes dissolved in the blood).

When the osmolarity of blood changes (it is more or less dilute), water diffusion into and out of the osmoreceptor cells changes. That is, the cells expand when the blood plasma is more dilute and contract with a higher concentration.

When the osmoreceptors detect high plasma osmolarity (often a sign of a low blood volume), they send signals to the hypothalamus, which creates the biological sensation of thirst. Osmoreceptors also stimulate vasopressin (ADH) secretion, which starts the events that will reduce plasma osmolarity to normal levels.

Renin–Angiotensin System-Mediated Thirst
Another way through which thirst is induced is through angiotensin II, one of the hormones involved in the renin–angiotensin system. The renin–angiotensin system is a complex homeostatic pathway that deals with blood volume as a whole, as well as plasma osmolarity and blood pressure.

The macula densa cells in the walls of the ascending loop of Henle of the nephron is another type of osmoreceptor; however it stimulates the juxtaglomerular apparatus (JGA) instead of the hypothalamus. When the macula densa is stimulated by high osmolarity, The JGA releases renin into the bloodstream, which cleaves angiotensinogen into angiotensin I. Angiotensin I is converted into angiotensin II by ACE in the lungs. ACE is a hormone that has many functions.

Angiotensin II acts on the hypothalamus to cause the sensation of thirst. It also causes vasoconstriction, and the release of aldosterone to cause increased water reabsorption in a mechanism that is very similar to that of ADH.

Note that the renin–angiotensin system, and thus thirst, can be caused by other stimuli besides increased plasma osmolarity or a decrease in blood volume. For example, stimulation of the sympathetic nervous system and low blood pressure in the kidneys (decreased GFR) will stimulate the renin–angiotensin system and cause an increase in thirst.

Regulation of Water Output
The majority of fluid output occurs from urination. Some fluid is lost through perspiration (part of the body’s temperature control mechanism) and as water vapor in expired air.
The body’s homeostatic control mechanisms ensure that a balance between fluid gain and fluid loss is maintained. The hormones ADH (antidiuretic hormone, also known as vasopressin ) and aldosterone play a major role in this.
If the body is becoming fluid deficient, increased plasma osmolarity is sensed by the osmoreceptors. This results in an increase in the secretion of ADH that causes fluid to be retained by the kidneys and urine output to be reduced.
Aldosterone is the major end-product of the renin – angiotensin system, and increases the expression of ATPase pumps in the nephron that causes an increase in water reabsorption through sodium cotransport.
ADH increases water reabsorption by increasing the nephron’s permeability to water, while aldosterone works by increasing the reabsorption of both sodium and water.

ADH Feedback
When blood volume becomes too low, plasma osmolarity will increase due to a higher concentration of solutes per volume of water. Osmoreceptors in the hypothalamus detect the increased plasma osmolarity and stimulate the posterior pituitary gland to secrete ADH.

ADH causes the walls of the distal convoluted tubule and collecting duct to become permeable to water—this drastically increases the amount of water that is reabsorbed during tubular reabsorption. ADH also has a vasoconstrictive effect in the cardiovascular system, which makes it one of the most important compensatory mechanisms during hypovolemic shock (shock from excessive fluid loss or bleeding).

Aldosterone Feedback
Aldosterone is a steroid hormone (corticoid) produced at the end of the renin–angiotensin system. To review the renin–angiotensin system, low blood volume activates the juxtaglomerular apparatus in a variety of ways to make it secrete renin. Renin cleaves angiotensin I from the liver -produced angiotensinogen. Angiotensin converting enzyme (ACE) in the lungs converts angiotensin I into angiotensin II. Angiotensin II has a variety of effects (such as increasing thirst) but it also causes release of aldosterone from the adrenal cortex.

Aldosterone has a number of effects that are involved in the regulation of water output. It acts on mineral corticoid receptors in the epithelial cells of the distal convoluted tubule and collecting duct to increase their expression of Na+/K+ ATPase pumps and to activate those pumps. This causes greatly increased reabsorption of sodium and water (which follows sodium osmotically by cotransport), while causing the secretion of potassium into urine.

Aldosterone increases water reabsorption; however, it involves an exchange of sodium and potassium that ADH reabsoption regulation does not involve. Aldosterone will also cause a similar ion -balancing effect in the colon and salivary glands as well.