Renin Angiotensin Aldosterone System (RAAS): Pathway, Functions & Terms
- Track Progress
- 0:05 The Control of Blood Pressure
- 2:26 Angiotensinogen & Angiotensin I & II
- 4:28 Control of the GFR
- 6:11 Aldosterone & ADH
- 7:48 Negative Feedback Mechanisms & Loops
- 10:36 Lesson Summary
The renin-angiotensin-aldosterone system is one of the most complex and important systems in controlling the blood pressure in your body. As we go over this system, you'll also learn about the many hormones involved in the control of your body's glomerular filtration rate and blood pressure.
The Control of Blood Pressure
I'm pretty sure you have seen or heard a commercial touting a new drug that helps to regulate something known as systemic hypertension, or high blood pressure, all over the body. Your body has an entire system that regulates blood pressure as well. It is actually built to counteract low blood pressure, or hypotension, instead of hypertension. You'll find out in this lesson that the main ways by which we can increase blood pressure is by constricting our blood vessels, increasing the amount of fluid in them, or both. Our body has a great way of doing the latter. Let's see how.
The Renin-Angiotensin-Aldosterone System (RAAS)
Your body has a huge system involved in the sensation and control of blood pressure not only within the kidneys but all over the body - especially in times of great need. This is in contrast to a smaller system called tubuloglomerular feedback, which you can think of as the system that senses and controls blood pressure and glomerular filtration rate within the kidneys on a moment-by-moment basis. When called upon, this smaller system can also rev up the really big system I'm about to get into. So what is this really big system?
Could I get a drumroll? The most important system involved in the regulation of systemic blood pressure, renal blood flow and glomerular filtration rate is called the renin-angiotensin-aldosterone system, or (RAAS) for short.
The Release of Renin
When systemic hypotension, or low blood pressure throughout the body, occurs, receptors in your blood vessels called baroreceptors sense this change. Cells of the kidney's juxtaglomerular apparatus get involved as well. Detection by one or both of these mechanisms leads juxtaglomerular cells in the kidneys to release an enzyme called renin. Renin is an enzyme released by the juxtaglomerular cells of the kidneys in response to low blood pressure, causing the transformation of angiotensinogen to angiotensin I.
Angiotensinogen & Angiotensin I
Angiotensinogen is a precursor protein made in the liver for a hormone called angiotensin I. Essentially, renin catalyzes a reaction that converts the angiotensinogen protein into angiotensin I, which is a precursor hormone that is converted to an active hormone called angiotensin II by an enzyme known as angiotensin-converting enzyme in the lungs. Wow, that was a mouthful! Let's break this down.
Here's how to remember what becomes what. Angiotensinogen's purpose is to serve as a precursor to angiotensin I. Angiotensinogen is cleaved, or broken apart, by renin. Since it's broken apart, it gets smaller and becomes shorter in name as well. Therefore, it's now called plain old angiotensin I. Angiotensin I decides to have a little kid and name it after itself. Therefore, when angiotensin I is converted in the lungs by an enzyme called ACE, it becomes angiotensin junior - or more technically, angiotensin II.
Angiotensin Converting Enzyme (ACE) & Angiotensin II
It bears repeating that the angiotensin-converting enzyme, or ACE for short, is an enzyme located mainly in the lungs that converts angiotensin I into angiotensin II. Once angiotensin II is made, it can have a big effect on the body. Namely, angiotensin II is a vasoconstrictive hormone that increases systemic blood pressure, renal perfusion pressure and the glomerular filtration rate.
Angiotensin II not only constricts blood vessels all over the body in order to increase systemic blood pressure, it also works in the kidneys in order to maintain blood pressure in the glomerulus so that the glomerular filtration rate stays normal even in the face of low blood pressure.
Control of the Glomerular Filtration Rate (GFR) by the RAAS
Let's see how this works with a familiar example. If you connect a hose to a faucet and turn the faucet on, a certain pressure will be exerted by the water on the walls of the hose. Likewise, blood running through the glomerulus (our hose) does the same thing. If the faucet is turned down a bit due to hypotension, there is less water running through the hose and therefore less pressure being exerted on the hose. If this were to happen in our glomerulus due to hypotension, this would be very bad. We need to maintain pressure in the glomerulus at a certain level if we want to filter our blood enough to stay alive.
To maintain pressure in the glomerulus and therefore keep the glomerular filtration rate steady, angiotensin II constricts both the efferent and afferent arteriole, but with a much greater effect on the efferent arteriole. Remember, the effect of angiotensin II is greater on the efferent arteriole. This means that the blood entering the glomerulus has a much harder time leaving it because the exit is far smaller than the entrance. This causes a backup of blood in the glomerulus, increases the pressure within it and, therefore, keeps the GFR at an appropriate rate.
In addition, angiotensin II increases the absorption of sodium in the renal tubule. Since water follows sodium, it increases the amount of fluid in the blood vessels, further causing an increase in blood pressure in addition to the vasoconstriction that already occurred.
Angiotensin does some other important things that you must remember. It causes the release of a hormone called aldosterone from the adrenal glands. Aldosterone is a hormone that increases the absorption of water from the distal convoluted tubule and collecting duct of the kidney's nephrons.
Aldosterone has many other functions, including the secretion of potassium into urine. However, for this lesson, you should understand that aldosterone causes the absorption of sodium out of the renal tubule's filtrate and into the blood. Since water follows sodium, more water is reabsorbed back into the blood in order to increase the blood pressure.
Anti-Diuretic Hormone (ADH)
As if constricting blood vessels and releasing aldosterone to retain water and sodium weren't enough, angiotensin II also causes the release of a hormone called anti-diuretic hormone, commonly called vasopressin, or ADH for short.
ADH is a hormone released from the posterior pituitary gland that causes an increase in blood pressure. ADH vasoconstricts our blood vessels, which causes increased blood pressure. It also increases water absorption from the distal tubule and collecting ducts. Now that you know what it does, it's easy to remember this because 'anti' in 'anti-diuretic' means 'against,' and 'diuretic' means 'excess urine production' that occurs thanks to water loss. Hence, ADH is against the loss of water in urine from your body!
Negative Feedback Mechanisms & Loops on the RAAS
Finally, you must understand that if the RAAS system was to run wild without any inhibitory control, it would actually kill you. This is why there are several mechanisms in place that try to control the RAAS system so that it doesn't go into overdrive. We'll go over some of the most important aspects of this inhibitory feedback system.
First off, increasing levels of angiotensin II are sensed by your body, and this by itself suppresses renin release. This is called an inhibitory feedback loop. As angiotensin II increases, renin decreases, which means angiotensin II also decreases since it depends on renin for its production.
Secondly, as blood pressure is restored back to normal thanks to vasoconstriction and water retention baroreceptors in your body's blood vessels sense the increased pressure and send signals to the juxtaglomerular cells to stop secreting renin. This signaling eventually stops the entire RAAS cascade. No renin means no angiotensin II and therefore no aldosterone or ADH either.
Thirdly, molecules such as nitric oxide and certain prostaglandins are released by your body to vasodilate (or expand) the same vessels angiotensin II is trying to constrict. Basically, these guys help to prevent angiotensin II from over-constricting the blood vessels.
Atrial Natriuretic Peptide (ANP)
Finally, there's an important hormone that counteracts the effects of the RAAS system. This hormone is called atrial natriuretic peptide, or ANP for short. Once your body senses increased blood pressure, (especially in the atria of the heart) increased sodium concentration (thanks to the hormones we just went over), and increased angiotensin II, ANP is secreted by the muscles of the heart. ANP will then directly stop the secretion of renin and aldosterone. It will also decrease sodium reabsorption and therefore by extension water reabsorption.
Furthermore, ANP will increase GFR in order to expedite the secretion of sodium and water out of the body. If we expedite the secretion of water out of the body, we will help to lower the blood pressure. In the end, all of these actions help to maintain blood pressure and glomerular filtration rate at a normal level by balancing out the effects of the RAAS system.
Phew. Was that confusing or what? Let's go over the most important points you must remember. I'll try to combine things when possible to help you see the big picture.
The most important system involved in the regulation of systemic blood pressure, renal blood flow, and glomerular filtration rate is called the renin-angiotensin-aldosterone system, or (RAAS) for short. This system will lead to the secretion of renin, which is an enzyme released by the juxtaglomerular cells of the kidneys in response to low blood pressure, causing the transformation of angiotensinogen to angiotensin I.
The angiotensinogen renin converts is a precursor protein made in the liver for a hormone called angiotensin I. The angiotensin I is itself a precursor hormone that is converted to an active hormone called angiotensin II by an enzyme known as angiotensin-converting enzyme in the lungs.
It bears repetition that the angiotensin-converting enzyme, or ACE for short, is an enzyme located mainly in the lungs that converts angiotensin I into angiotensin II. With this in mind, please remember that it's only angiotensin II that is the biologically active form of angiotensin, and it is a vasoconstrictive hormone that increases systemic blood pressure, renal perfusion pressure and the glomerular filtration rate.
Angiotensin II causes the release of a hormone called aldosterone from the adrenal glands. Aldosterone is a hormone that increases the absorption of water from the distal convoluted tubule and collecting duct of the kidney's nephrons. In addition, angiotensin II also causes the release of a hormone called anti-diuretic hormone, commonly called vasopressin, or ADH for short. ADH, if you recall, is a hormone released from the posterior pituitary gland that causes an increase in blood pressure. Finally, one of the most important substances involved in counteracting the RAAS system is known as atrial natriuretic peptide, or ANP for short.
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