the renin-angiotensin-aldosterone system is a system that gets activated when our blood volume drops and our blood pressure drops and the whole purpose of it is to increase blood volume increase blood pressure so let's have a look and see how this system works if you have a look renin-angiotensin-aldosterone three different terms and they're released in that particular order so the first thing we need to talk about itself is rennet now if you were to take the kidneys you should know that the filtration system is called the nephron and there's about 1 million nephrons per kidney now
the majority of the nephron sits in the cortex of the kidney but the loop of Henle and the collecting ducts sit within the renal pyramids also known as the medullary pyramids if I were to take a single nephron out and were to stick it here what you'll find is that there's an afferent arteriole which is blood coming in and then it turns into a capillary network called the glomerulus then an efferent arteriole coming out now what you need to be aware of is that your kidneys need to filter about 120 milliliters of blood per minute
or they need to create a 120 milliliters of filtrate per minute that means when this blood comes in of this blood it needs to get filtered into this glomerular capsule and 120 milliliters of what's now called filtrate is produced per minute that means about 180 liters per day of filtrate is produced however of that 180 liters that we produce per day we don't pay out all of that 180 liters as I'm sure you're aware we peered only 1% of that 1.8 liters so that means 99% of what we filter at the glomerulus is thrown back
into the body back into the bloodstream now this is important because the kidneys is basically weighing up exactly what we need what we don't need okay now this is why the kidneys must maintain this consistent what's called glomerular filtration rate of 120 mils per minute if your blood volume drops for example due to a bleed out so hemorrhage or Judas some sort of peripheral vaso violation which may happen due to anaphylactic shock for example your blood pressure drops and your blood volume drops now that means that the kidneys at the glomerulus will not be out
of filter that 120 milliliters per minute and this is a stimulus to release the first component of the renin-angiotensin-aldosterone system called renin now where is Renan specifically released from well let's have a look in the afferent arteriole the blood coming in there are some cells in the walls of the afferent arteriole now these cells are called juxtaglomerular cells also known as renin releasing granular cells so they're called jak-stat juxtaglomerular cells also known as granular cells granular cells now these are the cells that actually release renin now Renan is an enzyme okay it's not a hormone
it's an enzyme and it's released by the granular cells of the afferent arteriole okay now what stimulate this release I told you a drop in blood volume drop in blood pressure but how does it know this well it knows this because as the blood that's coming in if the blood volume has dropped and therefore blood pressure has dropped these juxtaglomerular cells or glimmer or the granular cells are actually baroreceptors and they pick up that drop in blood pressure and then they release renin so the first way renin is released first way that renin is released
is a drop in blood pressure in afferent arteriole that's the first way there's another way that really can be released now think about this if the blood pressure has dropped and the blood volume has dropped that means the Bloods moving through quite slowly with less of a force or push behind it so it comes through to the glomerulus gets filtered and they've created filtrate here now think about if the blood pressure's low blood volume is low this filtrate is going to move through slowly and if it moves through slowly remember that at the proximal convoluted
tubules this is where we reabsorb approximately 65% of all the stuff that gets thrown back into the body that includes sodium and then at the loop of Henle around about 15% is thrown back at the loop of Henle and the other portion understood the descending and a sending portions of the loop of Henle and then about 5% is thrown back at the distal convoluted tubule this is of sodium okay now if this filtrate is moving through slowly think about it there's more time for this salt to be pulled back into the body which means more
sodium gets taken out of the tubules and thrown back into the body which means by the time we reach the distal convoluted tubule is there going to be less sodium or more sodium there's going to be less sodium this is the next trigger to release renin but how for in the distal convoluted tubule and these cells are here well there's a cell type in the distal convoluted tubule that measure concentration they're called macula densa cells macula densa cells they measure concentration so the chemoreceptors and what they do is there's actually you can see that the
afferent arteriole is comes into close proximity with the distal convoluted tubule they're very close together an actual fact they're connected by connective tissue and this allows for a conversation to be had from the distal convoluted tubule to the afferent arteriole specifically the macula densa cells to the granular cells and therefore when these macula densa cells pick up a drop in sodium in the distal convoluted tubule they tell the granular cells to release renin so what's the second reason why we were released renin is a drop in sodium concentration in the distal convoluted tubule okay now
there's a third thing that stimulates the release of renin and it it is direct innervation from the sympathetic nervous system that's the fight-or-flight system think about that in terms of fight or flight we want to increase our blood pressure we want to increase our blood pressure why because it means our heart can deliver more blood to the muscle so it can fight or run away and so this is the third reason well the third way in which renin is released increased sympathetic nervous system innovation all right so the first thing you need to know is
what triggers the release of renin three things one a drop in blood pressure which triggers the granular cells to directly release renin in the afferent arteriole to a drop in sodium concentration in the distal convoluted tubule this is picked up by the macula densa cells which then speak to the granular cells to release renin and three the sympathetic nervous system directly innovates the granular cells to release renin so now we've spoken about how renin is released in the first instance we now need to talk about how the rest are released and how it actually increases
blood volume increases blood pressure well let's move over to this part of the diagram now now what I've just said to you is that Renan has been released from the kidneys now Renan is released from the kidneys into the systemic circulation it's floating around now the liver produces and also stores many proteins as well and usually if it's something that's stored and inactive it has the suffix og a n on the end of it and what the liver produces and stores is something called angiotensinogen again another protein angiotensinogen angeas referring to blood vessels Tinson refers
to pressure OG en tells you it's stored and inactive and what's going to happen angiotensinogen is released into the bloodstream and comes across Renan which I said is an enzyme what does this enzyme do well Renan chops off that OG en and create something called angiotensin one I'm just going to write a t1 angiotensin one what does angiotensin one do not too much it is a very slight vasoconstrictor but clinically doesn't really matter angiotensin one now is floating around now the thing is that angiotensin 1 as it floats around the bloodstream is inevitably going to
get to the lungs now the lung produces the most amount of an enzyme called angiotensin converting enzyme let's write that down I'll write it down up here NGO tensing converting enzyme I see a ace so it produces something called ace now think about what it does angiotensin converting enzyme it's going to convert angiotensin 1 into something called angiotensin 2 now this is what we're interested in angiotensin 2 angiotensin 2 is what we're interested in what does it do a couple of things first thing is that angiotensin 2 is a generalized vasoconstrictor it's predominately gonna straight
constrict arterioles which means the Bloods gonna back up back up back up and increase blood pressure so when you have a generalized vasoconstrictor what is the ultimate outcome for generalized vasoconstrictor it ends up increasing blood pressure what's the second thing that angiotensin 2 does well angiotensin 2 also goes to the efferent arteriole and when it gets to the affinity remember arterioles when you hear the word arteriole it's a small artery they have huge amounts of smooth muscle and so what angiotensin 2 does is it goes to this smooth muscle that's wrapped around the afferent arteriole
and it tells it to constrict what does that mean if these arterioles are constricting blood is backing up into the glomerulus that increases filtration rate which is exactly what we wanted because the stimulus was a decreased filtration rate right when that decreased filtration rate happened we had all the sodium get thrown back into the body and the sodium levels were low that was the trigger now we've got negative feedback we've fixed it up there's going to be no more trigger there so the second thing that angiotensin 2 does is it constricts the efferent arteriole and
what's the outcome for constricting the efferent arteriole increasing glomerular filtration rate which also increases the sodium in the distal convoluted tubule okay what else does angiotensin 2 do angiotensin 2 will also travel importantly all the way to the adrenal glands specifically it's going to travel to the cortex of the adrenal gland and stimulate it to release something called aldosterone the last part of the renin-angiotensin-aldosterone system aldosterone now what does aldosterone do aldosterone travels to the distal convoluted tubule and it tells the distal convoluted tubules to take the sodium that's present and throw it back into
the body now why would we want that if our blood volume is low and our blood pressure is low why would we want to throw more sodium back into the body well remember wherever sodium goes water follows therefore sodium back into the body sodium back into the blood water back into the blood increase blood volume that's the outcome so number three aldosterone from adrenal cortex and what's it do increases sodium reabsorption which ends up increasing blood volume which ends up increasing blood pressure what's the last thing that I want you to know that aldosterone up
angiotensin ii does well it travels to the hypothalamus now the hypothalamus is the master regulator of the endocrine system right and what that means is that endocrine system hypothalamus to pituitary glands anterior posterior the posterior pituitary gland has ADH antidiuretic hormone diuresis to urinate anti-diarrhea says to stop urinating so angiotensin ii tells ADH antidiuretic hormone to be released into the body and this will travel to the distal convoluted tubule and the collecting ducts and tell them to reabsorb more water into the body reabsorb more water into the body that's what ADH does this happens at
the distal convoluted tubule and collecting ducts why more water again more blood volume more blood pressure so the last thing I want you to know that angiotensin ii does stimulates the release of antidiuretic hormone from the posterior pituitary gland and this resulted in what resulted in increased water reabsorption which increased blood volume which increased blood pressure there you go what was the stimulus stimulus was dropping blood volume drop in blood pressure what was the outcome when you stimulate renin-angiotensin-aldosterone system increase in blood volume increase in blood pressure hope that makes sense
