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.
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.
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.
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.