Renal | Autoregulation (Updated)

what's up ninja nerds in this video we're going to be talking about renal autoregulation before we get started please if you guys benefit you like this video hit that like button comment down the comment section and most importantly subscribe alright engineers let's get into it all right ninja so let's start talking about renal auto regulation what is renal autoregulation it's just the ability of the kidney to modify its blood flow and modify the way how much blood flow it's getting modify the urine out putting away okay so how does it do that there's two particular mechanisms which the kidney regulates its blood flow regulates its urine output so on and so forth it does it by itself intrinsically and there's two particular mechanisms that the kidney does on its own without any assistance and that is called the first one is called the myogenic mechanism okay so the first one that we'll talk about is called the myogenic mechanism it's a pretty simple and very effective one the next one is actually regulated by the kidney tubules okay and it's called the tubulo glomerular feedback mechanism it's one heck of a name okay so we have the first one which is the myogenic mechanism and the second intrinsic mechanism is called the tubular glomerular feedback mechanism so these ones are again it's the kidneys ability that any blood flow that's coming to the kidney the kidney will sift through that and its design is to be able to make urine okay if the blood pressure is too high you'll end up making too much urine if the blood pressure is too low you won't make enough urine so how does the kidney be able to modulate it where you make an appropriate amount of urine it can do it intrinsically via these two mechanisms now the extrinsic mechanisms are a little bit different so the kidney has to it can do it but it needs a little assistance from things outside of it and what are those two things those two things the extrinsic mechanisms start kicking in whenever the blood pressure really becomes low these extrinsic mechanisms really really kick in whenever the blood pressure becomes precipitously low the first one that we'll talk about is called the sympathetic okay your sympathetic nervous system and then the second one here is called we're going to abbreviate this one because it's a heck of a thing i like to call it the renin angiotensin aldosterone adh system the rise okay so the renin angiotensin aldosterone adh system or axis if you will and again these are the different mechanisms that we're going to go into great detail of so let's start first with the myogenic mechanism and then work our way through understanding how the kidneys regulate its blood flow and then therefore urine output or glomerular filtration okay all right engineers so let's start talking about the different intrinsic mechanisms particularly the myogenic mechanism so myogenic muscle so there's going to be some muscle involvement here it's actually a really straightforward pretty simple process and so we're going to talk about two scenarios one is how the muscles of the afferent arterial kind of giving it away here modulate blood flow to the kidney or the glomerulus particularly whenever there's high blood pressure and how they do it whenever there's low blood pressure so here's the first thing i want you to remember we talked about this in glomerular filtration but basically the concept is that blood pressure is kind of a surrogate for glomerular hydrostatic pressure so whenever the blood pressure is higher you can say that there is a higher kind of a glomerular hydrostatic pressure if you will and if you remember glomerular hydrostatic pressure is the pressure inside of the capillaries that's exerted to push things like plasma and solute components out of the capillaries and into this thing called the bowman's capsule that's what it is so effectively the higher the glomerular hydrostatic pressure assuming all other things remain constant like the oncotic pressure capsular all that stuff like that we would say that there would be an increase in the glomerular filtration rate all right now that's what would happen you have a higher glomerular filtration you'd make more urine now your kidneys try to modulate this a little bit to where it's not too excessive well you're not making too much urine or that the pressure doesn't remain too high that you cause a lot of injury and you know exertion of effect on these actual glomerular capillaries so how does it do this all right whenever there is high blood pressure okay you know the structures here of this little diagram this is your afferent arterial this is the glomerulus we'll denote this with like a g here this is the efferent arterial this green thing here is called the bowman's capsule and this first part here of the tubules is called the proximal convoluted tubule here right well you know blood flow it moves through the afferent arterial and then exits out the efferent arterial whenever there's high blood pressure okay so there's high blood pressure we already know that it's going to cause higher glomerular hydrostatic pressure you'll cause more filtration to come out of these glomerular capillaries and more blood to come more urine to be made via an increase in glomerular filtration now how do we counteract this here's what happens as more higher blood pressure is occurring there's more blood that's flowing through there's higher pressure in the afferent arterial imagine we zoom in on one of those smooth muscle cells and look and see what happens here if there's higher blood pressure what this is going to do is this high blood pressure is going to exert a lot of force and pressure and stress and stretching on the smooth muscle cells of the afferent arterial so as a result these bad boys are going to have an increase in stretch well you know whenever they're stretched a lot they have these like channels here that are sodium channels that are very sensitive to stretch so whenever there's an increase in stretch these sodium channels open and the sodium will flood in when the sodium floods in that makes the inside of the cell super positive which is a stimulator to what's called the sarcoplasmic reticulum which is like a calcium storage within smooth muscle cells when this is stimulated it starts unloading that calcium into the smooth muscle cell like it's going out of style if there's lots of calcium inside of this smooth muscle cell from that increased stretch what's going to happen there's going to be more binding of myosin to actin and they'll be increasing contraction as a result of that when you cause more smooth muscle cells of the afferent material to contract it's going to induce what's called vasoconstriction okay so it's going to induce a vasoconstriction type of mechanism now imagine that from that high blood pressure these afferent arterioles just clamp down if they clamp down what does that do to the amount of blood the volume of blood that can run through the afar material little hole less volume so there's going to be a lower glomerular blood flow we'll put gbf here right that lower glomerular blood flow if less blood is flowing through here are you going to be able to make as much of that push as much of that plasma out here into the glomerular capsule capsule no so low glomerular blood flow will result in a lower glomerular filtration rate so as a result there'll be less filtration here and there'll be a lower glomerular filtration rate as the corrective or compensation or autoregulatory mechanism here okay so with that being said with low blood pressure it should be very easy now it's the exact opposite here low blood pressure means an effective lower glomerular hydrostatic pressure which would mean that there will be a lower gfr so how do we counteract that because if the blood pressure is low and this is where it's really the problem is when the blood pressure is low if the blood pressure is low we're not making urine that can cause a kidney injury right we don't want that so how does our kidneys try to help prevent that well it's pretty smart actually again to quickly recap here this is the this little diagram this is our afferent arterial efferent arterial this is our glomerulus here this is our bowman's capsule this is our proximal convoluted tube of the first part here right we have blood flowing through the afraid arterial exits via the efferent arterial now the blood pressure is low if there's low blood pressure that means that there's less force or stress or stretching of the afferent arterial so come back over here zooming in on a smooth muscle cell here if there is less stretch okay so there's a lower blood pressure that's less force and stretching on this actual smooth muscle cell a decrease in stretch those stretch receptors i mean the sodium channels that are very sensitive to stretch they're not going to be as sensitive now so now less sodium is going to enter in to these smooth muscle cells if less sodium enters into the smooth muscle cells there's less positive charge the sarcoplasmic reticulum ain't going to respond to no you know not as much positive charge so it's going to be like uh i'm not pushing calcium out and so because of that less calcium is present in the actual sarcoplasm that means less interaction between actin and myosin and that means less contraction another way that i want us to think about this is that there's less contraction that also means that there's kind of more relaxation of the muscle right it's kind of like the the you know the associated kind of opposite effect here less contraction meaning it's probably going to relax a lot more if the smooth muscles relax within this vessel we call this effectively vasodilation okay so we're going to effectively call this vasodilation now vasodilation imagine these blood vessels the affirmative kind of plumping up opening up really wide and allowing for a larger volume of blood more flow to run within that blood vessel as a result here now i'm going to have an increase right in the glomerular blood flow if i have an increase in the glomerular blood flow then i technically are going to have more volume running in here and i effectively should have more filtration and if that's the case i should have an increase in gfr or an attempt to increase the gfr through this mechanism when the blood pressure is low an easy way to summate all of this is what when the blood pressure is high it causes the gfr to go up how do we counteract that how do our kidneys do that they undergo vasoconstriction so high blood pressure triggers vasoconstriction causing low gfr summating the low blood pressure which is the more important thing low blood pressure leads to low gfr that's a problem because then the kidneys can't make urine that can lead to a kidney injury how does our kidneys protect that leads to vasodilation of the afferent arterial and an increase in the effective gfr that covers the myogenic now let's cover tubular glomerular feedback mechanism all right so we talked about the myogenic mechanism now let's talk about the tubular glomerular feedback mechanism so this one's a very cool one okay it can get it kind of complicated but we're gonna break it down to the simplest explanation all right so we have to talk about two scenarios what happens in this mechanism when the blood pressure is too high what happens when the blood pressure is too low it's kind of the same thing we talked about with the the myogenic mechanism but the same concept here as if we get to it is that a high bp increase in glomerular hydrostatic pressure effectively and ultimately it results in an increase in the glomerulation rate low blood pressure low glomerular hydrostatic pressure eventually it'll lead to a low glomerular filtration rate okay so that's kind of the end result here right so we can kind of effectively kind of follow this out here that again with our diagram here this is our affair arterial this is our efferent arterial this is our glomerulus this is our bowman's capsule this is our proximal convoluted tubule we won't have to explain it here for that one but high blood pressure right when things run from afferent to efferent material as it does that higher blood pressure you're going to have more filtration now here's what we've got to be really specific we are having a higher gfr right now we're having an increase in our glomerular filtration rate effectively but what are we filtering we already talked a little bit about this we're filtering out plasma or filtering out solutes but this mechanism is really really specific for a very particular molecule called sodium chloride so it's very sensitive for sodium chloride so we say that technically when there's a high gfr you're actually causing more sodium chloride to get filtered as well so more sodium chloride is filtering into the actual bowman's capsule and then the proximal convoluted tubule right and the same concept here and again this is high bp high glomeral filtration more sodium chloride is actually being filtered into the kidney tubules again afferent arterial efferent arterial glomerulus bowman's capsule proximal completed tubule here blood flows here exits here but should filter here at the glomerulus low bp low glomerular filtration rate that effectively means that less solute and less plasma is filtered but the more particular one is sodium chloride that less sodium chloride is filtered here so that's what i want you to take away from this first part here regardless of high bp or low bp what we can kind of say with this mechanism at this point is high bp high gfr high sodium chloride excretion into the kidney tubules low bp low gfr low sodium chloride excretion into the kidney tubules okay let's continue to follow that down though so let's say that we take the sodium chloride and we move down right so let's continue down here we have just an expanded version of kind of our nephron right so here we're going to say this is the afferent material this is the efferent arterial so afferent arterial efferent arterial here okay this is the bowman's capsule proximal convoluted tubule this is the loop of henle this is the ascending so this is your descending ascending so that's why we call just the loop of henle distal convoluted tubule and then the collecting duct right the real points that i want you to focus on is the distal convoluted tubule really okay so we have here high blood pressure we're filtering off lots of sodium chloride where does most of the sodium chloride get reabsorbed in the proximal convoluted tubule but let's say just imagine that the sodium chloride transporters they got saturated they're like man i can't keep up with all of this sodium chloride that's out here i can't juggle all of this so some of the sodium chloride kind of escapes past the proximal convoluted tubule it moves down through the loop of henle and it finally gets to this distal convoluted tubule where you have some special cells here some special sodium chloride sensors in the distal convoluted tubule what are these cells here called let's write them in purple so that they shine shine bright like a diamond these are called macula densa cells and these are special sodium chloride sensors whenever they sense that there is a high amount of sodium and a high amount of chloride they are very sensitive to that and they release a very particular type of molecule in response to that okay this molecule is called what this molecule we're actually going to have it released over here on this side because it's going to interact with a very particular part in this nephron okay it's going to release a molecule called adenosine and adenosine is going to act on a particular part here in the afferent arterial that we have to discuss down here okay but we'll do that in just a second what i want you to recap here is high bp high gfr high sodium chloride excretion to the kidney tubules if there's lots of sodium chloride in the proximal convoluted tubule a lot of it can actually not get reabsorbed and if a lot of it gets down to the distal convoluted tubule cells it causes the macula densa cells to sense that and release adenosine let's talk about the opposite scenario if we go here again afferent arterial efferent arterial this is our bowman's capsule proximal convoluted tubule this is the distal convoluted tubule loop of henle and then again the collecting duct with more focus here on the distal convoluted tubule again blood will flow through the afar material out the efferent material and you should get some filtration here at the glomerulus we had low bp low gfr so there's low amounts of sodium chloride here in the proximal convoluted tubule that gives the proximal convoluted tubule plenty of time to reabsorb tons and tons of that sodium chloride so if we were to trace this sodium chloride down as it goes throughout all of this processing it finally gets to the distal convoluted tubule these macula densa cells okay those special sodium chloride sensors there's going to be very little sodium chloride by the time it gets to the distal convoluted tubule so there's low amounts of sodium and there's low amounts of chloride by the time it gets here the macula densa cells in response to that actual low sodium and low chloride release two particular molecules and these are called pgi2 and nitric oxide and these will act on particular components within the afferent arterial as well so super quick recap high bp high gfr high sodium chloride excretion in the kidney tubules high amounts of sodium chloride get to the distal convoluted tubule macula densa cells release adenosine low bp low gfr low sodium chloride excretion into the kidney tubules less sodium chloride gets down to the dct macula densa cells sense the low sodium chloride released pgi-2 in nitric oxide now what does adenosine do in this area of the inferior material and what does pgi 2 and nitric oxide do in this area of the affair material that's what we have to discuss next so let's go over here all right so we're here and we had let's say that we just kind of had it released here we kind of show that it was released here was the adenosine the adenosine can do two things one is it can act on the smooth muscle cells right so this is our afferent arterial this is our efferent arteriole it's going to act on the afferent arterial and cause it to clamp down okay it's going to cause it to clamp down if the actual afferent arterial clamps down or undergoes vasoconstriction so what would be the response here here if we were to kind of write this out we're going to have a vaso constriction of the what afferent arterial what does that mean then if it constricts its smaller diameter less blood flow is running through there that results in a lower glomerular blood flow that means less filtration is going to occur if there's less filtration that's a lower glomerular filtration rate that means that less sodium chloride is being filtered less sodium chloride being filtered is the opposite of the original issue we fixed the issue we lowered the gfr we lowered the sodium chloride excretion beautiful that's fixed something else it does is very interesting so here we're going to have adenosine here like it was released from the mat here we'll put macula densa uh cells right we'll abbreviate mdc maculodenzo cells they release the adenosine the adenosine acts there causes the vasoconstriction there's another thing it does adenosine will act on these uh these cells that are present around the afferent arterial you know these cells that are present around the eighth energy they're very specialized cells they're called j g cells they stand for juxtaglomerular cells not a chance of this world i'm writing that out the jg cells are very special because they contain granules of what's called renin now renin activates the randon angiotensin aldosterone system and their whole goal is what i want you to remember here is to increase blood pressure right and increase sodium chloride reabsorption all that stuff if the issue was i had high blood pressure would i want the jg cells to release renin effectively increasing blood pressure no so adenosine is actually going to inhibit the jg cells from releasing renin and so there will be no renin release and we won't activate the renin-angiotensin aldosterone adh axis okay but let's come over here now you guys are already getting like you already know what's gonna happen right it has to be the opposite here we release those macula densa cells released what's called pgi2 and nitric oxide that's going to act on again what is this structure here this is the affair material efferent arterial here blood flows here exits here and it should filter in the middle of the glomerulus pgi2 and nitric oxide are going to act on the smooth muscle cells of the afferent arteriole and when it does that it causes these smooth muscle cells to undergo a relaxation causing them to vasodilate so effectively you're going to cause vasodilation of what the afferent arterial that's going to widen it up more blood flow can run through there so there'll be effectively an increase in the glomerular blood flow more blood flowing through will have more filtration if there's an increase in the glomerular filtration rate you're going to increase the amount of sodium chloride that's being excreted that's fixing the issue where you had the low gfr and the low sodium chloride now that's one part the other part here is that the pgi2 and nitric oxide will act on these cells over here the jg cells again the jg cells are responsible for releasing renin what was the original issue the blood pressure was low what does ren and what it will want to do increase your blood pressure so what i want the jg cells to become stimulated so that they can release rain and effectively increasing the blood pressure yeah so i'm going to trigger that process and so it's going to stimulate the jg cells and cause them to release renin and so we'll put like an up over here so that you know that and then a down arrow here so that you know that right increase in renin it'll activate the whole renin angiotensin aldosterone system indirectly whenever there's low bp okay that covers the tubular glomerular feedback let's talk about the sympathetic nervous system all right ninja so let's talk about the extrinsic mechanisms for renal autoregulation so this is again the the kidney is starting to now need some assistance from some other systems and this is where the nervous system kind of kicks in so really this extrinsic mechanism doesn't really kick in until the blood pressure is like relatively low so these this this two extrinsic mechanisms they're really more particular that we really need to know we're not going to go over them when the hot when there's high blood pressure it's easy we can quickly blow through it but i want us to focus more on these two extrinsic mechanisms when the blood pressure is low because that's when these pathways are a little bit more involved okay so the sympathetic nervous system will really become involved whenever like your systolic blood pressure is really plummeting okay so as it starts to become relatively low so the point where the mean arterial pressure starts becoming like less than like 65 really okay so less than 60 if you really wanted to remember that we can say really map is a is a measure of perfusion right so when the map starts becoming like less than 65 millimeters of mercury we're not perfusing the kidney as well and that can cause kidney injury so the sympathetic nervous system kind of tries to kick in really whenever our blood pressure is getting really low because it has to allow for say okay kidney you're important but you're not as important as the heart the brain muscles other tissues that need this blood flow so i'm going to kind of have to take blood flow a little bit away from you and divert it to a little bit more of the principal important organs and so that's kind of the the issue that we'll run into here with the sympathetic nervous system so let's kind of talk about this whenever there's low blood pressure right we know that effectively when we talk about it with the kidney that low blood pressure is going to lead to a low gfr right and that low gfr is going to lead to effectively it can lead to a low urine output and the problem with this is that this can lead to kidney injury if you have less blood flow going to the kidney not only are you decreasing the urine output but you can cause kidney injury and that unfortunately the sympathetic nervous system doesn't respect that we have other mechanisms that'll try to protect that but it will do its best to try to get blood flow to increase so how does it do that when the blood pressure is low you know there's specialized types of receptors like baroreceptors that are present here within kind of the carotid sinus and the aortic sinus and they pick up whenever there's low blood pressure and these there's nerves that carry these signals here okay we have like the vagus nerve and then we also have the glossopharyngeal nerve and the glossopharyngeal nerve okay so we'll have the vagus nerve and then we'll have the glossopharyngeal nerve they're picking up sensations from these bare receptors so whenever the bp is low it's going to trigger these baroreceptors and it's going to cause these two nerves to kind of send signals to our brainstem particularly in the medulla when it sends these signals to the medulla the medulla will say hey i'm getting less signals from cranial nerve nine and ten especially from the bare receptors the blood pressure must be low that's not good let me ramp up the sympathetic nervous system centers here and so what it does is it'll activate particular sympathetic nerve fibers and the thoracic part of the spinal cord and other parts here and this will do a couple things one is it'll cause the release of an increase in the release of norepinephrine and increase in the epinephrine in the heart and what it's going to do is it's going to act on the nodal systems and when it acts on the nodal system it'll attempt to increase your heart rate because you know when you increase heart rate that increases what effectively cardiac output which will try to increase your blood pressure that's the goal it's also going to increase your contractility of the heart so it's going to increase the stroke volume if you increase these two things effectively that should increase the cardiac output and increase the blood pressure because the whole goal is if i increase the blood pressure i can increase the profusion or more blood to go to the kidney so that the kidney doesn't get injured okay i'll do my best but at this point in time my goal is getting blood flow to other tissues the heart the muscles the brain those have to take precedence okay but that's one of the mechanisms that it'll do the other mechanism here and again here's an important thing to remember what are the receptors that are actually responsible for increasing heart rate this is the beta 1 receptor so simulate the beta 1 receptors that are present on the sa node av node but it'll also stimulate the beta 1 receptors that are present on the contractile myocardial tissue okay that's important so beta 1 receptors there so again stimulating the beta 1 receptors for increase in chronotropic action increasing the activity of the beta 1 receptors increasing inotropic action contractility now the sympathetic nervous system fibers also will do another thing they'll act on the alpha one receptors so what are these here called these are called here we'll kind of put like a little receptor here these are called your alpha one receptors and these are present on the what is this afferent arterial efferent arterial blood flow moves from afar material to efferent material right remember what i told you that unfortunately the sympathetic nervous system he don't respect the kidney he don't respect them so what he says is i got to get blood pressure up unfortunately kidney i tried to do it through this mechanism to perfuse or perfuse you a little bit but unfortunately i need blood flow to go to other organs and so it releases norepinephrine it releases epinephrine which will bind onto the alpha one receptors of the afferent arterial and cause vasoconstriction so what's the effect here it's going to cause vaso constriction if i vasoconstrict the afraid arterials how much blood flow is going to be able to move through there not very much and so there'll be a decrease in the glomerular blood flow and effectively a decrease in the glomerular filtration rate you're probably like zac i thought the goal was to try to increase the gfr it is that's the goal but unfortunately in a sympathetic crisis where your blood pressure is really low the sympathetic nervous system don't don't respect the kidneys and so it says hey i gotta try to get blood flow to other organs like the heart the muscles the brain so i might have to take it from the kidney unfortunately so that's one thing that can happen here right now the other thing that happens within the sympathetic nervous system is not only is there alpha one receptors that are present here on the um the smooth muscle of the afferent arterial but guess where else they're present on the alpha one receptors that are present within uh vessels all over the place so we have alpha one receptors that are on kind of our peripheral vessels here so here's an alpha one receptor what will happen is these fibers like if we were to kind of track this down here it's going to get too messy so just imagine here that these fibers here we'll do it like this so it doesn't get too crazy that's not bad actually so we're going to release out here the epinephrine and the norepinephrine and they're going to act on not only the alpha 1 receptors of the afferent arterial but let's just call these the systemic vessels so systemic arteries it's going to act on these vessels here on that alpha-1 receptor and induce vasoconstriction of multiple systemic vessels if you cause vasoconstriction of multiple systemic vessels what that does is it increases the systemic vascular resistance and if you increase the systemic vascular resistance you increase the blood pressure so the whole goal if you're getting the point here is that the sympathetic nervous system wants to increase blood pressure that would be nice if it would help the kidney but unfortunately it says hey your kidney i got to reduce a little bit of blood flow to you by constricting the afferent arterial but it also constricts all arterials that are alpha-1 receptors are present on okay now so far what do we have sympathetic narcissism causes increase in heart rate increase in stroke volume increasing cardiac output blood pressure through the beta 1 receptors acts on the alpha 1 receptors here of the afferent arterial causing vasoconstriction reducing gfr acts on the alpha and receptors of the systemic vessels causes increase in systemic vascular resistance increasing blood pressure the last thing here is you have cells that are present in the affair and arterial and they have beta 1 receptors that are present here and again the increase in epinephrine the increase in neural epinephrine will bind on to the beta 1 receptors on these particular cells and trigger the release of a very particular hormone these cells you guys already know them we wrote them over here we'll write them in purple these cells here are called your jg cells and again what does the jg cells do whenever they're stimulated release epinephrine norepinephrine they stimulate the beta-1 receptors they trigger the release of renin what does renin do you guys know we'll talk about in a second it activates eventually a molecule called angiotensin ii and angiotensin ii is going to do a bunch of different mechanisms that we're not going to go ahead and talk about now because we're going to talk about in a second here but this is what i want you guys to get the overall point of so to quickly recap sympathetic nervous system gets activated when the blood pressure is really low what does it do first thing increases your heart rate increases your stroke volume to increase cardiac output blood pressure second thing causes the vasoconstriction of the afr materials to get more blood flow to other organs not the kidney unfortunately other organs are a little bit more high priority third thing causes vasoconstriction of systemic arterials via the alpha one receptor to increase blood pressure and the fourth thing is it triggers renin release from the beta-1 receptors on the kidney okay all of this would be the exact opposite if the blood pressure was high right you wouldn't have as much of this sympathetic effect you'd have lower heart rate lower stroke volume lowering the blood pressure you'd have less alpha one receptor vasoconstriction so you'd have more gfr you wouldn't have renin release and you wouldn't have this vasoconstriction of the vessels here in the periphery you'd have vasodilation so everything that we said for low bp it'd be the exact opposite for high bp okay now that we covered this let's cover the final mechanism the most important one of them all the reynon angiotensin aldosterone adh axis all right engineers the last one renin angiotensin aldosterone adh axis this is this is the best one it's the most important one really out of all of these again we're going to focus on the low bp but it's going to be easy we'll talk about that for high bp and it's actually like one particular hormone that i want you to remember so thankfully it's not too bad okay first thing you have low blood pressure right why is this an issue okay we already know all this stuff this this should honestly be so dang easy at this point low bp low glomerular hydrostatic pressure that leads to a low gfr right low gfr that's kind of a problem right we're not making much urine because of that so if we were to kind of look here at like the kidney here okay and again we have the afferent arterial here we have the efferent arterial here and again we know that blood flow through here through here exits and there should be some filtration process here in the middle now if you have low blood pressure okay guess what there's some special cells that we've talked about before that not only do they are they sensitive to like adenosine to prostate cyclin nitric oxide the sympathetic nervous system all of that but they're also just sensitive on their own to blood pressure changes particularly whenever either the blood pressure is higher the blood pressure is low so we're going to kind of highlight here here's your jg cells okay they're going to be hearing that affair in arterial whenever the blood pressure is low so yeah low bp these jg cells respond to that they say man there's some low blood pressure that's not good i need to try to get the blood pressure up so what i'm going to do is is i'm going to release a molecule called renin because again what was the issue that low bp was resulting in lower glomerular hydrostatic pressure it was resulting in lower glomerular filtration rate right so we have to try to be able to fix this in some way as well as increase the blood pressure so that we can try to perfuse the kidney a little bit more we're going to try to some mechanisms here right so when the renin is released renin is kind of like a really cool enzyme your liver makes a very particular type of protein here it's one heck of a name but this protein that the liver makes is called angiotensinogen and what happens is renin is going to act like an enzyme and it's going to actually kind of cleave a couple of amino acids off of angiotensinogen when it cleaves angiotensinogen it converts it into a molecule called angiotensin one angiotensin one will then move to a capillaries within the lungs and you know within the lungs there's a very special enzyme that the lungs the capillary endothelium within the lungs have which is called ace angiotensin converting enzyme and what this enzyme does is it stimulates the conversion it cleaves off a couple amino acids of angiotensin one and converts him effectively into what's called angiotensin ii now this is our money maker here this is where all of it starts to really just happen angiotensin ii does so many different things what are some of the things that he does okay first one let's kind of drag him over here so the first thing is we're going to kind of see what it does here to your central nervous system the central nervous system has a very particular structure in this area the hypothalamus and then it has a structure that hangs here called the pituitary gland right when this stimulates the hypothalamus it stimulates the posterior pituitary and triggers the release of a very special type of hormone called adh so there's going to be an effective increase in this hormone it actually stimulates particular cells within the hypothalamus that trigger the release of adh from the posterior pituitary adh is a very special hormone it's also called vasopressin antidotic hormone but what it does is is it acts on the cells in the collecting duct you know the cells within the collecting duct uh they're very very impermeable to water but what happens is when adh is present it puts these little aquaporins present inside of the actual tubular membrane and then what happens is water can actually funnel into these actual tubular cells and into the actual bloodstream so effectively we get an increase in water reabsorption in the blood and if there's an increase of water in the blood that's going to increase your blood volume and if you increase your blood volume you increase your blood pressure what was the issue low bp if we increase the bp we can actually get more blood flow to go to the kidney so that the kidney can increase its gfr effectively man that's pretty cool right all right what else angiotensin ii can also you know another thing it also can do with the hypothalamus if you really want to remember here it can also just make you thirsty and if you have an increase in thirst you'll drink more water you drink more water you increase your blood volume you increase your blood pressure and increase the gfr right so it's kind of same kind of concept here but anyway it also can act on the adrenal cortex you know the adrenal cortex okay so we'll put here the adrenal cortex particularly what's called the zona glomerulosa you know the cells that make a particular hormone called aldosterone here we'll put zg zone glomerulosa triggers the release of a hormone called aldosterone now aldosterone likes to work on a very particular area which is also relatively impermeable to sodium and water naturally and this is the distal convoluted tubule right this was the collecting duct okay the collecting tubule the collecting duct this is the distal convoluted tubule this portion here aldosterone acts on these distal convoluted tubule cells and makes them permeable to sodium and makes them permeable to water so then you reabsorb sodium and you reabsorb water into the bloodstream so now i'm going to get more sodium and water into the bloodstream if you increase sodium and you increase water into the bloodstream you effectively increase blood volume if you increase blood volume you increase blood pressure you increase blood pressure you should get more blood flow to the kidneys and increase the gfr man it's making sense right all right what else another thing that the angiotensin ii does is it acts on the kidneys okay so it's gonna act on the kidneys itself right and it works in a very particular way two particular ways so here we're gonna have again the afferent arterial on this end the efferent arterial on this end angiotensin ii will bind on to these angiotensin ii receptors that are present on the efferent arteriole and when angiotensin ii binds onto these receptors it causes these this vessels the efferent arterial to undergo vasoconstriction so that's the result of this it's going to cause vasoconstriction but very very particular here of the efferent arterial if you squeeze the efferent turn now remember blood flows through the eighth variant likes to exit through the efferent material imagine that the efferent material is really small so less blood can escape from the glomerulus more blood will stay in the glomerulus if more blood stays in the glomerulus then more of it can be filtered out there's a longer transit time and so because of that you are going to increase the glomerular filtration rate it's kind of like a nice little protective mechanism that angiotensin ii has pretty cool right all right another thing that it's going to do angiotensin 2 also acts on cells within the beginning part of the nephron you know this is the proximal convoluted tubule well what it does is it also is going to act here so here's angiotensin ii acting on the proximal convoluted tubule it'll actually cause these cells to increase their reabsorption of sodium and water so if i reabsorb more sodium and water into the actual bloodstream i increase sodium i increase water i increase blood volume i increase blood pressure again if i increase blood pressure i increase perfusion to the kidney increase the gfr so it's pretty cool mechanism that angiotensin ii here has on the actual kidneys now some books say that it does act on the afferent arterial but what you should remember is that the angiotensin ii effect on the efferent arterial is much greater than the effect on the afferent arteriole and thank goodness for that because there at least is some protective effect there for the kidneys okay we're almost done here with the aspect of angiotensin ii now angiotensin ii also is a very very potent vasoconstrictor very potent so if we look at like your systemic arterials or your systemic vessels here we'll just put arterials but you know your systemic vessels here particularly arteries it's going to act on these vessels okay again the angiotensin ii receptors and when it does that again this is angiotensin ii here it's going to cause these vessels to really really clamp down and so it's going to induce a very impotent vasoconstriction when it causes this vasoconstriction the overall effect is that you increase your systemic vascular resistance now and if you increase your systemic vascular resistance you increase the blood pressure you should be able to increase your bp increase your perfusion to the kidneys and increase gfr that's all of the effects here the only other thing that we have to think about now is something very interesting okay the opposite effect when there's high bp when there's high bp this entire thing here just doesn't work we don't release brandon we don't cause angiotensinogen to be converted into angiotensin one angiotensin ii and all the effects of angiotensin ii don't occur here okay and if that doesn't happen then we're not going to have all of the things that we just talked about occur it's a pretty straightforward kind of process here the only other thing that i do want you to remember is that when there is an increase in blood pressure it can cause the heart to release a very particular type of molecule from the atria and it's called atrial natural peptide an atrial naturatic peptide will just basically here's what i want you to remember oppose or block any function of angiotensin ii so here's what i want you to think about if someone said what's the function of angiotensin ii all the opposite i'm sorry if anybody said what's the function of atrial natural peptide you say it's the opposite of angiotensin ii so watch this intranatural peptide is going to block each part here if it blocks angiotensin ii here it will not lead to adh release if there's no adh release you won't reabsorb sodium and water you'll actually urinate out lots of sodium and water okay and then because of that you'll have less blood volume in the body and then again they'll try to lower your blood pressure it's going to block the release of aldosterone atrium nitrate peptide will block out aldosterone release you won't reabsorb sodium and water from the distal convoluted tubule it'll cause more sodium and water to be released into the urine you'll have less blood volume and less blood pressure on the kidneys it's going to prevent the angiotensin ii from binding on to the efferent materials it's not going to undergo vasoconstriction if it doesn't undergo vasoconstriction it won't have this higher gfr if you will it'll try to lower the gfr it'll inhibit sodium and water reabsorption in the proximal convoluted tubule and cause more sodium and water to be released into the urine right and again it's going to lower your blood volume and then last but not least angiotensin ii is also going to try to cause vasoconstriction of the blood vessels atrial natural peptide will cause vasodilation of the blood vessels lower your systemic vascular resistance and lower your blood pressure man we good all right engineers that covers renal autoregulation all right ninja nerds in this video we talk about renal autoregulation i hope it made sense i hope that you guys did enjoy it as always ninja nerds until next time [Music] you

Channel: Ninja Nerd

Views: 96,864

Keywords: Ninja Nerd Lectures, Ninja Nerd, Ninja Nerd Science, education, whiteboard lectures, medicine, science

Id: 2HMPe3799QI

Length: 48min 42sec (2922 seconds)

Published: Mon Sep 06 2021