renin angiotensin aldosterone system

The point of this system is to regulate systemic blood pressure. This is executed mainly by the kidneys and the adrenal glands. I will first discuss the cascade and then the inputs leading to and affecting it, and its own effects on the system.

The liver maintains a high level of angiotensinogen in the blood. It is a large molecule, a small part of which is cleaved by renin to produce angiotensin I. This circulates through the blood until it encounters ACE, primarily in the lungs. This converts angiotensin I to angiotensin II, thereby activating it. The presence of angiotensin II in the bloodstream is sensed by the adrenal cortex, which then secretes aldosterone into the plasma.

Some of these hormones have effects on the system, as does angiotensin II, while others, such as angiotensin I, are only intermediates in the cascade. See the individual nodes of these items for more detail.

Below is a decent example of how plasma volume fluctuation can activate this system.

A decrease in plasma volume will cause an increase in the activity of renal sympathetic nerves, a decrease in arterial pressure, and a decrease in glomerular filtration rate and flow to the macula densa. The latter causes the macula densa to see fewer electrolytic ions. All of the above stimulate the juxtaglomerular cells to secrete more renin, thereby increasing its concentration in the plasma. By the system described above, this yields an increase in plasma angiotensin II, and therefore aldosterone. This increase in plasma aldosterone increase sodium reabsorption in the cortical collecting ducts, thereby decreasing the amount that leaves the kidneys via the ureters. Where sodium goes, water follows, and thus, less water is secreted, mainting plasma volume.

This sort of response might occur in case of large loss of blood or in dehydration.