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Renin-Angiotensin-Aldosterone System (RAAS) – Regulation of Ambulatory Blood Pressure (ABP)

by Thad Wilson, PhD
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    00:00 The next neurohumoral factor that is going to come into play is the renin-angiotensin- aldosterone system. Here, the RAAS system is sensed first by a change in mean arterial blood pressure. So let's take the example of a fall in mean arterial blood pressure. As blood pressure falls, the afferent arteriole that goes into the glomerular capsule will sense this fall in pressure.

    00:33 It releases a substance called renin. Renin then changes a liver plasma protein called angiotensinogen in the angiotensin I. Angiotensin I is then converted through angiotensin- converting enzyme, also abbreviated as ACE, into angiotensin II. There is ACE throughout the whole body but we talk about it primarily in the lungs because all of your circulation out of the right side of the heart travels through your lungs and so a lot of the conversion takes place in your lungs. Once you have angiotensin II, that is now an active molecule that can undergo various physiological functions. It directly acts on the kidney and causes increases in aldosterone.

    01:36 Aldosterone will directly relate to increasing sodium reabsorption in the distal tubule. If you reabsorb more sodium and more water, you're going to end up increasing your blood volume which increases your preload, which then increases your cardiac output, which then increases your mean arterial pressure and that should raise mean arterial pressure back to normal levels.

    02:08 So just like the baroreflex responding to a decrease in mean arterial pressure, increased mean arterial pressure through cardiac output and systemic vascular resistance, the renin-angiotensin-aldosterone system only works through cardiac output to increase mean arterial pressure. Angiotensin II, I mentioned, has some direct effects. These direct effects are in terms of changing blood volume through the sodium retention as well as some retention of water more indirectly because as you retain sodium water will follow. It stimulated aldosterone and we talked about that in the renin-angiotensin-aldosterone system. Angiotensin II though also increases your drive to drink or your thirst. This will allow you to intake more water to increase blood volume. Finally, angiotensin II does one other thing and that is it stimulates antidiuretic hormone also knows as arginine vasopressin to be released. An arginine vasopressin antidiuretic hormone has its own set of actions. Angiotensin II directly increases systemic vascular resistance and decreases venous compliance. What this is going to allow is constriction of blood vessels on the arterial side will change systemic vascular resistance, constriction of veins decreases venous compliance. So both of these are constrictions even though one is a change in systemic vascular resistance and the other is a change in venous compliance.


    About the Lecture

    The lecture Renin-Angiotensin-Aldosterone System (RAAS) – Regulation of Ambulatory Blood Pressure (ABP) by Thad Wilson, PhD is from the course Vascular Physiology.


    Included Quiz Questions

    1. Liver
    2. Lungs
    3. Adrenal gland
    4. Kidney
    1. Reabsorption of sodium
    2. Reabsorption of magnesium
    3. Reabsorption of sodium and excretion of water
    4. Reabsorption of calcium and excretion of potassium
    5. Reabsorption of potassium

    Author of lecture Renin-Angiotensin-Aldosterone System (RAAS) – Regulation of Ambulatory Blood Pressure (ABP)

     Thad Wilson, PhD

    Thad Wilson, PhD


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