Excretory and Digestive Systems - MCAT Biology

The signal to increase water reabsorption in the nephrons comes from antidiuretic hormones and aldosterone. The urine volume also decrease in an attempt to retain the fluids already present in the body. Since the body is trying to conserve the fluids it has and there are no incoming fluids, the blood volume should not increase.

Juxtaglomerular cells respond to low levels of sodium and secrete renin in response, which results in the release of aldosterone from the adrenal cortex. Aldosterone, as a result, will increase sodium reabsorption from the collecting duct. This will in turn increase blood pressure, however, the direct role of the cells themselves is to regulate blood osmolarity.

Vasopressin acts on the collecting duct in order to increase its permeability to water. This results in more water being reabsorbed, and increases blood pressure.

Aldosterone increases the reabsorption of sodium from nephron filtrate.

The reabsorption of sodium leads to reabsorption of water, which makes the urine more concentrated. Increasing aldosterone production would lead to increased blood pressure, since more water is retained in the blood stream.

Antidiuretic hormone, also known as vasopressin, increases the reabsorption of water from the collecting duct. It increases the permeability of the collecting duct, which allows water to be reabsorped and makes the urine more concentrated.

You can remember what antidiuretic hormone does by remembering that diuetics increase urine production; therefore an ANTIdiuretic will decrease urine production.

Aldosterone is released from the adrenal cortex and acts on nephrons to increase water and sodium retention. Aldosterone directly affects the synthesis of sodium ion channels and sodium-potassium pump proteins in the nephron, actively leading to sodium retention and indirectly leading to water retention based on increased blood osmolarity. Antidiuretic hormone (ADH), on the other hand, works by just retaining water without directly affecting sodium retention.

In a severely dehydrated patient, the kidneys will be acting to preserve water in the body. Renin is secreted by the kidneys, and is the starting enzyme for a cascade that stimulates the release of aldosterone. Aldosterone raises the blood pressure of the body by acting on the distal tubule, and antidiuretic hormone (ADH) is responsible for making the collecting ducts permeable to water, thus concentrating the urine. Because of this, we would expect that renin levels would be higher than normal in a dehydrated patient.

The passage outlines the role of angiotensin converting enzyme (ACE) in the renin-angiotensin-aldosterone system (RAAS). Because ACE inhibitors act on the enzyme that converts angiotensin I to angiotensin II, we would expect renin and angiotensin I to remain high because they are present before the ACE step in the RAAS pathway. The hormones present after ACE action, including angiotensin II and aldosterone, however would decrease with ACE inactivation, as would sodium reabsorption. The result is generally lower blood pressure.

We can see that inhibiting the action of ACE would cause buildup of renin and angiotensin I, and a decrease in angiotensin II, which would result in a failure to retain water.

The juxtaglomerular apparatus in the distal tubule monitors the filtrate that passes by to sense increases or decreases in blood volume. Granular cells in the apparatus secrete the enzyme renin, which initiates a cascade that ultimately produces aldosterone. Remember that aldosterone acts on the distal tubule to stimulate sodium reabsorption and potassium secretion.

Secretion of renin allows the conversion of angiotensinogen to angiotensin I. Angiotensin-converting enzymes (ACE) change angiotensin I to angiotensin II in the lungs, which then stimulates the adrenal cortex to release aldosterone and increase blood volume.

As mentioned from the passage, carbonic anhydrase inhibitors will alkalize the urine and make the blood more acidic. Therefore, the opposite will occur if one were to overstimulate the enzyme.

The main function of the Loop of Henle is to establish a concentration gradient so that water can be reabsorbed from the collecting duct and avoid being lost as urine. Although the ascending limb does absorb water, this water would be lost as urine if it were not for the concentration gradient established in the medulla of the kidney. Neither sodium nor potassium is absorbed in the Loop of Henle.

Together, Bowman's capsule and the glomerulus make up the renal corpuscle. Blood flows through the glomerulus, where high hydrostatic pressures force plasma through the fenestrations of the glomerular endothelium into Bowman's capsule. The substance that ends up in the capsule is called the filtrate, which then moves to the proximal tubule. Proteins, glucose, and ions are secreted from the proximal tubule back into the blood.

The collecting duct is impermeable to water and is not particularly sensitive to aldosterone. Instead, aldosterone, a steroid hormone produced by the adrenal cortex, acts primarily at the distal tubule to increase sodium reabsorption, potassium secretion, and ultimately water reabsorption to increase blood pressure. The distal tubule absorbs Na+ and Ca2+, not HCO3-.

The correct path of filtrate through a nephron starts in the renal corpuscle, which is comprised of the glomerulus and Bowman's capsule. Filtrate then passes through the proximal convoluted tubule, where the majority of reabsorption takes place. It then travels through the descending and ascending limbs of the Loop of Henle, creating the counter current multiplier gradient that will allow urine to be concentration in the collecting duct. From the Loop of Henle, filtrate enters the distal convoluted tubule for final reabsorption before entering the collecting duct and being trasported to the bladder.

The renal artery is used to carry blood into the kidneys. Filtrate originates from the renal artery, but it is not a part of the nephrons.

The kidney uses all three of the following processes: filtration, secretion and reabsorption. All three of these processes aid in allowing the body to filter waste products from the blood while retaining nutrients, salts, and water when needed.

Filtration occur when filtrate is separated from blood in the renal corpuscle. Reabsorption is the removal of ions from the filtrate to retain salts. Secretion is the input of salts to the filtrate to eliminate them. All of these processes occur in the nephrons.

The Loop of Henle creates a countercurrent multiplier system. As the filtrate descends through the Loop of Henle, water leaves the filtrate and is reabsorbed, making the filtrate very concentrated. When the Loop of Henle ascends, salt ions leave the filtrate and are reabsorbed making the filtrate less concentrated. This creates a strong concentration of ions in the interstitial fluid toward the bottom of the loop, as compared to the concentration at the top. When filtrate flows down the collecting duct, this gradient helps concentrate the urine by removing water.

The ascending and descending limbs of the Loop of Henle are responsible for creating a countercurrent multiplier system, which concentrates urine and allows water and electrolytes to passively diffuse down their concentration gradients.

All the other options are part of the nephron, but are not responsible for the process of urine concentration. The glomerulus and Bowman's capsule are responsible for collecting and producing initial filtrate from the blood, and form the renal corpuscle. The proximal convoluted tuble is the initial site of reabsorption.

A renal afferent arteriole is directed toward the glomerulus, while a renal efferent arteriole is directed away from the glomerlus. If the radius of the afferent arteriole is increased, there is more flow through it toward the glomerulus, and if there is a smaller radius in the efferent arteriole, there is a resultant back pressure in the glomerulus. This is can be imagined as trying to squeeze a high-pressure hose through a small pipe. This pressure increases the force within the glomerulus to increase filtration, and subsequently increase reabsorption.

Antidiuretic hormone (ADH) secretion has a neglible effect on the radius of renal arterioles. Blood flow to the kidney is increased when afferent arteriole radius is increased (this also increases the arteriole flow).

The purpose of the proximal tubule is to reduce the amount of filtrate in the nephron. The proximal tubule does alter the solute concentrations in the filtrate, but it does not alter the osmolarity of the filtrate. This is because the proximal tubule is where reabsorption of solutes, proteins, and glucose takes place. Meanwhile, drugs and toxins are being secreted into the filtrate. Essentially, the volume of filtrate in the proximal tubule decreases, but the filtrate remains isotonic to the blood.

It is important to understand how urine is concentrated as it travels through the nephron. The proximal convoluted tubule does not alter the osmolarity of the filtrate, the loop of Henle increases the osmolarity of the filtrate, and the distal convoluted tubule lowers the osmolarity of the filtrate. In the absence of antidiuretic hormone, the collecting duct will be impermeable to water, preventing it from leaving the filtrate and resulting in more dilute urine. With the collecting duct impermeable to water, the filtrate will be most concentrated at the bottom of the loop of Henle.

Antidiuretic hormone (ADH), also known as vasopressin, increases the permeability of the collecting duct to water. This allows a more concentrated urine to be excreted, because water is being lost from the urine to the kidney tissue before excretion. The gradient created by the reabsorption of ions from the loop of Henle means that the interstitium is hypertonic to the collecting duct. If the permeability of the collecting duct to water is increased, we would expect water to flow out of the collecting duct. We would expect ADH levels to increase with dehydration in order to preserve water.