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.

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.

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.

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.

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.