Excretory Physiology - AP Biology

ATP is needed to help power the excretion of urine through the nephron. The thick ascending limb, for example, is thicker because it contains more mitochondria than other portions of the loop of Henle. The changing environment of the nephron is a product of the continual reabsorbtion of water and ions throughout the excretion process.

The renal medulla contains the loops of Henle and collecting ducts. As filtrate travels toward the interior of the kidney, the increased ion concentration (hypertonic environment) aids in the reabsorption of water. This ion gradient is established by ion flow from the concentrated filtrate in the descending limb toward less concentrated blood and interstitial fluids.

When the filtrate enters the bottom of the loop of Henle, it is at its highest concentration. As the filtrate travels up the thin ascending limb, sodium is passively reabsorbed as it flows down its concentration gradient to exit into the less concentrated interstitium.

Sodium is then actively pumped by the sodium-potassium-chloride co-transporter in the thick ascending limb, which transports all three ions out of the filtrate into the interstitial fluid (reabsorption). Later, in the collecting duct, a sodium/potassium transporter is used to further reabsorb sodium, while excreting potassium into the urine.

As the nephron dips into the medulla in the descending limb of the loop of Henle, water passively diffuses out of the filtrate. This concentrates the solutes in the filtrate. As the filtrate enters the ascending limb of the loop of Henle, the tube becomes impermeable to water and ions are pumped into the interstitium. This creates a gradient of higher ion concentration in the medulla and dilutes the filtrate.

The diluted filtrate enters the distal convoluted tubule, where water and ions are reabsorbed. This slightly increases the filtrate concentration before it enters the collecting duct. As the filtrate flows down the collecting duct into the renal medulla, the ions in the interstitium act to draw water out of the duct (dependent on the presence of antidiuretic hormone). The result is a highly concentrated urine product after the filtrate travels down the collecting duct, all due to the ion gradient established by the loop of Henle.

The loop of Henle is essential for creating an ion gradient in the renal medulla (the inner part of the kidney). In the descending limb of the loop of Henle, water is removed from the filtrate by aquaporin proteins (water channels). The result is a highly concentrated filtrate at the bottom of the loop.

The filtrate then enters the thick ascending limb, which is permeable to sodium ions. The sodium ions rush out of the filtrate into the interstitium, which now has lower concentration than the filtrate. When the collecting duct later travels through the high concentration of sodium ions that have accumulated in the renal medulla from the thick ascending limb, water is pulled out of the filtrate into the interstitium. This allows for the final step in concentrating the urine before it travels to the bladder.

The loop of Henle serves the crucial function of creating an ion gradient in the renal medulla by fluctuating the reabsorption of water and ions. In the descending limb, water is removed from the filtrate and enters into the interstitium, resulting in a highly concentrated filtrate. This filtrate then enters the ascending limb. The ascending limb is not permeable to water, but is permeable to sodium ions. The result is a massive efflux of sodium ions, which exit the filtrate and enter the interstitium. Sodium pumps amplify this process by continuing to remove sodium from the filtrate. The filtrate becomes more dilute, but the interstitium in the renal medulla is highly concentrated. When the filtrate enters the collecting duct, this gradient helps pull water out of the filtrate, allowing it to reach a maximum concentration before being transported to the bladder.

If the ascending limb of the loop of Henle were permeable to water, this process would be impossible and the filtrate would not be concentrated in the collecting duct.

Diuretic drugs promote the production of urine. One drug, known as furosemide, inhibits transport of both sodium and chloride in the ascending limb of the loop of Henle. This mechanism of action prevents the maintenance osmolarity gradients that promote the reabsorption of water, resulting in more dilute urine. If the gradient is lost, then water is not drawn out of the filtrate as it travels through the collecting duct and the result is a larger volume of dilute urine. Antidiuretic hormone, secreted from the posterior pituitary, works to promote the reabsorption of water in the collecting duct, which concentrates the urine and conserves water.

Parietal cells in the stomach release hydrochloric acid, activating pepsin and aiding in digestion. This creates a highly acidic environment in the stomach that could be harmful to other regions of the body. When the stomach contents, or chyme, is transported out of the stomach and enters the small intestine it must be neutralized. The first segment of the small intestine is the duodenum, where digestive enzymes from the pancreas are secreted to help digest fats and proteins.

Along with these enzymes, bicarbonate is secreted by the pancreas into the small intestine. The bicarbonate reacts with the remaining acid, producing water, salt, and carbon dioxide.

The functional unit of the kidney is the nephron. Blood is filtered into the nephron to create filtrate. As the filtrate flows through the nephron tubules, its concentration is tightly regulated and ions and water are added and removed. The end result is a highly-concentrated filtrate that is transported to the bladder for excretion.

Neurons are the functional unit of the nervous system, not the kidney. Sarcomeres are the basic contractile unit of skeletal muscle, and chief cells are specialized stomach cells that secrete digestive enzymes, such as pepsinogen.

Ammonia is highly water-soluble and can be toxic to cells at low concentrations due to presence of its ammonium ion, which can interfere with oxidative phosphorylation. Ammonia is small and can easily diffuse through cell membranes, making it easy to excrete. Essentially, there is a trade off of easy excretion and toxicity levels.

For aquatic animals, however, toxicity is negligible due to the large volume of water available to dilute ammonia wastes. The high solubility of ammonia wastes and the abundance of water solvent allow for the ammonia to be transported out of cells in an very dilute concentration, without harming the organism. This allows aquatic organisms to conserve energy, compared to terrestrial organisms that must convert ammonia wastes to other forms.

Amphibians and mammals convert ammonia to urea, which can be excreted with less water, but must still be relatively dilute. These animals release liquid wastes from the body, resulting in water loss, but conserve energy compared to organisms that continue to convert urea into uric acid. Birds and reptiles excrete uric acid, which requires very little water waste, but uses a larger amount of energy in conversion. This is beneficial to animals that may not have ready access to fresh water.

There is a key trade-off between energy consumption and toxicity in the excretion of nitrogenous wastes. Ammonia is the simplest form of the waste product, and requires very little energy to produce; however, it is highly toxic and must be diluted to extremely low concentrations in order to be safe to the cells. Many aquatic animals excrete ammonia because of their proximity to water. Access to large amounts of water means that these organisms can safely excrete dilute ammonia without needing to use energy in conversions.

Terrestrial animals, with less access to water, excrete urea or uric acid. These wastes are derived from ammonia, but require an input of energy for the conversion. They are less toxic and require less water loss for dilution, making them ideal for animals that must conserve fluids. Uric acid is the least toxic of the nitrogenous wastes, but also requires the greatest energy investment.

Alcohol decreases the activity of antidiuretic hormone (vasopressin). A diuretic increases the production of urine and thus, inhibition of this _anti_diuretic hormone results in an increase in the production of highly diluted urine.

Alcohol does not block the flow of fluids through the kidney tubules.

Proteins would not be found in the urine because these molecules are too large to pass through the glomerulus of the nephron of the kidney. They would be filtered out and remain in the bloodstream. Meanwhile, all of the other compounds would be present in normal urine.

Antidiuretic hormone (ADH) is responsible for concentrating the urine. This is accomplished by making the collecting duct permeable to water, and allowing it to passively diffuse into the renal medulla. Alcohol will inhibit the function of ADH, which means that the urine will be less concentrated because water is unable to leave the collecting duct, thus also increasing the volume.

Water is reabsorbed at various times during the excretion process as it passes through the nephron, in order to maintain proper ion levels. It is not, however, reabsorbed as urine ascends through the thin and thick ascending limbs in the loop of Henle. Rather, this region only involves ion reabsorption and urea secretion.

Sodium is reclaimed through passive transport in the thin ascending limb and is reclaimed by active transport in the thick ascending limb, distal tubule, and collecting duct. Each location of sodium resorption uses a different transport protein and mechanism.

The filtrate and surrounding interstitial fluid are at their highest osmolarities at the bottom of the loop of Henle. As the filtrate continues on, it enters the thin ascending limb of the loop of Henle, which is impermeable to water. As the thin ascending limb moves up through the nephron into areas with a lower osmolarity, sodium flows down its concentration gradient to exit the filtrate. At this point, the filtrate is at a lower osmolarity than the surrounding interstitial fluid due to sodium flowing out and water being barred from flowing in.

As filtrate travels down the descending limb of the loop of Henle, water passively leaves the filtrate as the descending limb passes through portions of the nephron that contain a more concentrated interstitial fluid. Water always travels from places of high water concentration (low osmolarity) to low water concentration (high osmolarity); thus, the water will passively flow out of the filtrate and into the interstitium.

As the loop of Henle turns, the filtrate passes through the thin ascending limb, which is impermeable to water, but permeable to ions. As the limb passes through less concentrated areas of the nephron, sodium passively flows down its concentration gradient from the filtrate to the interstitial fluid. At no point during this process is water actively transported.

In the presence of antidiuretic hormone (ADH), water is reabsorbed and the urine is concentrated. Antidiuretic hormone plays the biggest role on the collecting duct and distal tubule, allowing water to diffuse into the medulla by increasing the production of aquaporin proteins. These proteins become embedded in the membranes of the nephron epithelium and allow water to pass through the usually impermeable cells.

The other important regulator of water balance is aldosterone, which works by a different mechanism. Aldosterone increases production of sodium channels, allowing sodium to exit the filtrate in the distal tubule. Water diffuses to follow the reabsorbed sodium ions.

One of the key adaptations of the mammalian kidney is the ability to conserve water through reabsorption and excretion of concentrated urine. This is accomplished by maintenance of an osmolarity gradient, suitable for extracting water from the filtrate. The two primary solutes are sodium, which is deposited in the renal medulla by the loop of Henle, and urea, which crosses the epithelium of the collecting duct in the inner medulla. The increased osmolarity of the interstitial fluid enables water to be extracted and conserved through aquaporin proteins in the collecting duct.

Vasopressin, also called antidiuretic hormone (ADH), is part of the hormonal control of urine excretion and functions to enhance reabsorption of water, limiting the excretion of water in urine. Vasopressin is released when osmoreceptor cells in the hypothalamus detect a rise in the osmolarity (solute concentration) of the blood above a threshold level. Upon release, vasopressin reaches the kidney and binds to receptors on cells in the collecting duct, which stimulates release of aquaporin water channels from storage vesicles within the cells. Aquaporin channels are selectively permeable to water, and allow the flow of water out of the filtrate/urine. This water is then reclaimed by the body and used to increase blood volume, increase blood pressure, and reduce blood osmolarity.