In this video, we're going to be going over the renin-angiotensin-aldosterone system, also known as the RAS. And I'll be honest, this one can be a little bit of a doozy. There are a lot of steps in this mechanism, it has multiple effects on the body, and there is some kind of big terminology to keep track of. So I would encourage you to take your time with this video, pause it if you need to, and you and I will get through this together, so no worries. So as you may have heard previously in your AMP course, the renin-angiotensin-aldosterone system is the body's main mechanism for increasing blood pressure. So our main stimulus here is going to either be sympathetic activity or the detection of low blood pressure. And I know that at first glance, those can kind of seem like opposites; we think like fight or flight increased blood pressure. But keep in mind, from the perspective of a kidney which would receive less blood flow during sympathetic activity, these are basically the exact same thing. So we're going to go through how the mechanism works. And one nice thing to keep in mind is that it basically is named in the order that substances will appear. So first, we're going to see renin, then angiotensin, and then aldosterone. So keep that in mind as we go through these. So first up, our blood pressure is going to decrease. We're going to have less blood flow to our kidneys, whatever happens. And then as a result of that, our macula densa cells will detect a low glomerular filtration rate because they're going to be receiving less sodium chloride. So our macula densa cells will then signal to our kidneys, hey, we have to release the enzyme renin into the bloodstream. So the kidneys release renin, and there is the first piece of our name. So then renin is going to go to the liver where it converts angiotensinogen into angiotensin 1. Angiotensin 1 will then travel to our lungs where it gets converted into angiotensin 2. And angiotensin 2 is going to be really the main player here. So there is the angiotensin piece of our name. And angiotensin 2 has widespread effects on the body in order to increase blood pressure. So it's going to be directly increasing blood pressure. It's going to be increasing blood volume, as well as having a direct effect on glomerular filtration pressure and rate. So it's going to be very busy. Now we're going to start over here talking about how it directly impacts systemic blood pressure. And it does that through the vasoconstriction of systemic blood vessels. You can imagine we're going to have constriction here. So it's kind of like taking a garden hose that's already on. You took that hose and kind of squeezed it and constricted it. You can imagine how the water coming out of it is going to be coming at a much higher pressure, and that's what's happening in your body there. But right off the bat, we have this increase in blood pressure as a result of that vasoconstriction. Now, moving over to this middle piece, we're also going to be increasing blood volume, which remember increasing blood volume is going to indirectly impact our blood pressure by increasing it as well. So we have this dotted line here to kind of symbolize how increasing blood volume will also help increase blood pressure. And, angiotensin 2 increases blood volume in 2 ways. So we're going to start over here. And that angiotensin 2 is going to be promoting the reabsorption of sodium in the proximal tubule of our nephron. Remember, reabsorption is when we take a substance out of the filtrate and put it back into our bloodstream. So by promoting the reabsorption of sodium, that is also going to cause the reabsorption of water by osmosis. We'll talk about this in some upcoming videos, but long story short, basically, water wants to follow high electrolyte concentration. So if water sees a whole bunch of sodium leaving the filtrate and going back into the blood, water wants to follow it. So we're going to have a whole bunch of water entering our blood, which of course will increase our blood volume. So that's what's happening in the proximal tubule. Now, angiotensin 2, we're going to move over here now, angiotensin 2 is also going to promote the release of aldosterone, the last piece of our name there. And aldosterone increases the reabsorption of sodium as well. But it is going to do so in the distal tubule and the collecting duct. And so we're also working kind of in this opposite end of the nephron, and that's going to have the exact same effect. It's going to cause water reabsorption by osmosis there as well. So now we have in basically the majority of our nephron, we have increased water reabsorption. We have a whole bunch of water entering our blood which will, of course, impact our blood volume. You can imagine o