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Fluid and Electrolyte Balance
The kidneys are essential for regulating the volume and composition of bodily fluids. This page outlines key regulatory systems involving the kidneys for controlling volume, sodium and potassium concentrations, and the pH of bodily fluids.
A most critical concept for you to understand is how water and sodium regulation are integrated to defend the body against all possible disturbances in the volume and osmolarity of bodily fluids. Simple examples of such disturbances include dehydration, blood loss, salt ingestion, and plain water ingestion.
Water balance is achieved in the body by ensuring that the amount of water consumed in food and drink (and generated by metabolism) equals the amount of water excreted. The consumption side is regulated by behavioral mechanisms, including thirst and salt cravings. While almost a liter of water per day is lost through the skin, lungs, and feces, the kidneys are the major site of regulated excretion of water.
One way the the kidneys can directly control the volume of bodily fluids is by the amount of water excreted in the urine. Either the kidneys can conserve water by producing urine that is concentrated relative to plasma, or they can rid the body of excess water by producing urine that is dilute relative to plasma.
Direct control of water excretion in the kidneys is exercised by vasopressin, or anti-diuretic hormone (ADH), a peptide hormone secreted by the hypothalamus. ADH causes the insertion of water channels into the membranes of cells lining the collecting ducts, allowing water reabsorption to occur. Without ADH, little water is reabsorbed in the collecting ducts and dilute urine is excreted.
ADH secretion is influenced by several factors (note that anything that stimulates ADH secretion also stimulates thirst):
1. By special receptors in the hypothalamus that are sensitive to increasing plasma osmolarity (when the plasma gets too concentrated). These stimulate ADH secretion.
2. By stretch receptors in the atria of the heart, which are activated by a larger than normal volume of blood returning to the heart from the veins. These inhibit ADH secretion, because the body wants to rid itself of the excess fluid volume.
3. By stretch receptors in the aorta and carotid arteries, which are stimulated when blood pressure falls. These stimulate ADH secretion, because the body wants to maintain enough volume to generate the blood pressure necessary to deliver blood to the tissues.
In 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. The net effect on urine excretion is a decrease in the amount of urine excreted, with lower osmolarity than in the previous example.
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