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11.03 Renin Angiotensin Aldosterone System (RAAS)

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  1. Control of Blood Pressure (BP)
    1. Juxtaglomerular apparatus
      1. Juxtaglomerular cells at afferent arteriole
      2. Macula densa cells from DCT
    2. Stimuli
      1. Hyponatremia – decreased sodium levels in blood
      2. Low BP in afferent arteriole
        1. Decreased perfusion to kidneys
    3. Effect
      1. Juxtaglomerular apparatus releases the enzyme Renin

Nursing Points


  1. Mechanism—Renin angiotensin aldosterone system
    1. Renin gets released
    2. Angiotensinogen in blood reacts with renin
      1. Creates Angiotensin 1
    3. Angiotensin 1 circulates through lungs
      1. Combines with angiotensin-converting enzyme (ACE)
      2. Converts Angiotensin 1 to Angiotensin 2 , which does the following:
        1. Vasoconstriction → increased BP
        2. Stimulates Aldosterone release
          1. Sodium reabsorption in DCT
            1. Chloride follows sodium
          2. Water follows NaCl by osmosis
            1. ↑ Blood volume
            2. ↑ BP
        3. Secretes ADH from posterior pituitary gland
          1. Increases water reabsorption at collecting duct
            1. ↑ Blood volume
            2. ↑ BP
        4. Increases SNS activity
    4. Once BP or sodium levels restored, renin stops being released → stops Angiotensin and Aldosterone action → stops water retention → levels off the BP
  2. Can see this response with:
    1. Hyponatremia
    2. Hypotension
    3. Shock
    4. Heart Failure
    5. **See individual lessons**


Betts, J.G., et al. (2017). Anatomy and physiology. Houston, TX: OpenStax, Rice University. Retrieved from

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Video Transcript

In this lesson we’re going to talk about the renin angiotensin aldosterone system. This is the way that the kidneys help to regulate and control blood pressure.
Inside the kidneys there’s a structure called the juxtaglomerular apparatus. The prefix juxta- means next to. So this is a structure next to the glomerulus. This involves juxtaglomerular cells in the afferent arteriole and macula densa cells in the distal convoluted tubule. You can see how anatomically they back up to each other here. These cells will detect certain conditions within the bloodstream to start this process. There are three main stimuli that will start this process. One is hyponatremia or low sodium levels in the blood. Another is low blood pressure in the afferent arteriole or decreased perfusion to the kidneys. So essentially if the kidneys aren’t getting enough blood flow, or sodium levels are low, it will start this process. When the juxtaglomerular apparatus is stimulated, it causes release of the enzyme Renin. The release of Renin is what causes the cascade known as the Renin-Angiotensin-Aldosterone system.

So let’s look at the Renin Angiotensin Aldosterone System – or the RAAS one step at a time. First, we get a stimulus – again it could be hyponatremia, low blood pressure, or low perfusion to the kidneys. That stimulates the release of the enzyme renin. Now, in our blood already circulating, is a protein called Angiotensinogen. When that comes in contact with Renin, it gets converted to Angiotensin I. Angiotensin I circulates in the bloodstream until it gets to the lungs, where it comes in contact with an enzyme called the Angiotensin Converting Enzyme, or ACE. That enzyme, as its name says, converts Angiotensin I to Angiotensin II. Angiotensin II is what does ALL the work here – it’s our powerhouse. So let’s look at the 4 main things that angiotensin II does in our body. First, is that it causes a release of Aldosterone. Aldosterone goes to the kidneys and causes retention of sodium. Anytime sodium gets reabsorbed, chloride and water will follow – so we also see water retention. When we retain more water, our blood volume increases, which can increase our blood pressure. The 2nd thing Angiotensin II does is causes the release of ADH from the pituitary gland. ADH stands for antidiuretic hormone – diuresis means to get rid of water or urinate – so if it’s ANTI diuretic then that means we’re NOT going to get rid of water, so we’re going to retain it. Again, if we retain water our blood volume goes up, which increases our blood pressure. 3rd, we see peripheral vasoconstriction – so this is the blood vessels out in our body like in the extremities that will constrict to increase the pressure and bring more blood back to the kidneys and to the heart. Lastly we see increased Sympathetic Nervous System activity. That will increase our heart rate and blood pressure – review the Autonomic Nervous System lesson for more about that. So – ultimately, all of these things are going to work together to help increase our blood volume, which increases our blood pressure, and improves the blood flow to the kidneys. Remember the initial stimuli – right here is where we see the improvement of sodium levels, and all the rest will help improve the flow to the kidneys. When that happens, it reverses that initial stimulus and stops this process so that everything can level off. This cycle happens all the time in the body so that we maintain a normal blood pressure all the time.
Okay – let’s recap. The stimuli for the Renin Angiotensin Aldosterone system are low blood pressure in the afferent arteriole, low perfusion to the kidneys, or hyponatremia. Those things are sensed by the juxtaglomerular apparatus, which stimulates the release of renin. Renin converts angiotensinogen to angiotensin I which is converted to angiotensin II by angiotensin converting enzyme, or ACE, which is in the lungs. Angiotensin II is the powerhouse – it causes the release of Aldosterone and ADH, vasoconstriction, and increased sympathetic nervous system activity. Aldosterone and ADH will cause increased sodium and water retention, which increases blood volume, and all of these things together will help to increase blood pressure and improve the flow to the kidneys so these stimuli can stop and everything can level off.
This system – this renal regulation of blood pressure is going to come up a LOT as you start to learn about disease processes, especially anything that has to do with the heart and cardiac output and the kidneys. One great example is heart failure – so make sure you check out those lessons to see how this impacts those patients. Check out all the resources attached to this lesson as well. Now, go out and be your best selves today. And, as always, happy nursing!