all right engineer in this video we're going to talk about blood pressure but specifically we're going to spend some time talking about the compensation mechanisms that are occurring within our body whenever we are exhibiting low blood pressure okay so we're going to talk about that we're going to specifically again focus on what are the compensation mechanisms that are occurring within the body hormonal neural chemical very I different causes and how that again how our body can compensate for that to bring our blood pressure back up okay so what what would actually trigger this to happen Okay we said low blood pressure but let's get a little bit more specific okay what did we actually consider to be low blood pressure or another term that you might have heard is called hypo tension hypotension is low blood pressure and specifically we categorize when whenever you're systolic blood pressure okay the actual ventricular pressure the amount that your ventricles are trying to expel specifically the left out of the Harden into the great vessels whenever it is less than 100 millimeters of mercury so whenever your systolic blood pressure is less than 100 mm of mercury we classify that as hypotension now generally what will happen is is you're going to have certain compensation mechanisms that are going to occur so we're going to talk about it in general we're going to say what are the things that are happening whenever our blood pressure drops below 100 millimet of mercury and maybe even significantly lower maybe down to like 80 millim of mercury okay in certain situations where it can get really low like in hypmic shock so let's talk about all these different mechanisms okay well first off how does our body detect this changes in blood pressure through Barrel receptors pressure receptors where can you find those little suckers you're going to find them right over here we've talked about these guys throughout a series of our videos right and we know that we're going to have these special types of barrel receptors or pressure receptors located in two areas okay one is actually going to be right here in What's called the aortic sinus so you're going to find a bunch of these little purple guys here these are all Barrel receptors and they have these sensory AER nerve endings here and these sensory AER nerve endings are again they're going to be located within in this area the aortic sinus so again what were these guys here called they're called Barrow receptors and they're located in aortic sinus okay now these barel receptors are very specific and the reason why is these bear receptors that are actually taking this information and detecting the changes in the blood pressure this one located within the ortic sinus is carried on a specific cranial nerve and that cranial nerve is cranial nerve 10 which is also called the Vagas nerve so this is aarant fibers General visceral aeren fibers of the vagus nerve and they're going to detect changes in the blood pressure within the aorta there's other ones and they're located right here at this bifurcation point you see this right here this is actually right here this vessel moving in this area this one right here is called the left common cored artery so this one here is called the left common cored right that's what this bad boy right here is called what happens is he comes into this area this little kind of like bifurcation point and splits into an external and into a internal cored artery right right at that bifurcation Point you're going to notice there is actually going to be some barar receptors located within What's called the cored sinus so what is these ones right here called these right here are your Barrel receptors in cored sinus okay sweet deal these guys are going to be picking up the changes in blood pressure let me explain how but first off before I do that what is this guy these sensory aparent nerve endings that are actually with connected as the bar receptors on the cred sinus this sensory aparium information is carried on cranial nerve 9 which is the glossop fenial nerve okay so the aortic sinus has bare receptors which are carried on the sensory a fibers of vegus the bare receptors and the corate sinus are going to be carried on the sensory AER fibers of the glossop fial nerve or cranial nerve 9 and they'll take this information into a special nucleus in the medulla that we'll talk about called the nucleus of tractus solitarius okay now quick question is how do these Barrel receptors respond to changing blood pressure let me say I kind of zoom in on that sensory nerve ending real quick so I'm going to zoom in real quickly on like a little sensory nerve ending so let's say that this is the axle right or in this case this part here is the peripheral process this is the sensory nerve vending it has little channels here and what happens is whenever your blood pressure is high it's going to stretch the actual vessel walls when it stretches The Vessel walls what happens is it activates this channel to bring sodium ions in whenever the blood vessel is being stretched so whenever the blood vessel is being stretched it activates these bear receptors which opens up these channels on the bear receptor sensor nerve indings and allows for sodium to flow in but what did we say was the actual situation we said that this person had a systolic blood pressure less than 100 millim of mercury maybe even very significant to about 80 is that going to be stretching the blood vessel walls no if it doesn't stretch the blood vessel walls is they going to open up these channels no is sodium going to flow in no so these channels are not going to be open they're going to be closed what's going to happen to the actual potentials the action potentials carry down this axon it's going to not occur or it's going to be very very little or very slow so we can say slow or no APS okay Action potentials carried on these nerves so let's get this clear low blood pressure there's going to be very little stretch on the blood vessel wall very little stretch on the blood vessel wall is pretty much we can say not going to stimulate this vagus nerve so we like to say it as though it's really inhibiting the nerve okay it's inhibiting the sensory AER fibers of the vagus nerve it's also inhibiting the sensory aeren fibers of the bare receptors that are located within the corate it's carried on the glossop frenal nerve when they take this information up to the nucleus of tractus solitarius the nucleus of tractus solitarius kind of sifts through that information as it sifts through that information it says oh crap the blood pressure is low I have to respond to this correctly so he says I got three centers to choose from what are those centers this maroon Center here this maroon Center here is called the cardiac exelator center I'm going to put that as CA the cardiac exelator center this Center is connected with our sympathetic nervous system so the cardiac accelator center is connected with your sympathetic nervous system this brown one here is called the Vaso motor Center I'm going to put VM the vasom motor Center and the vasom motor Center is also connected with our sympathetic nervous system and this last one here this green one is actually called the cardiac inhibitory Center but really this is where the dorsal nucleus of Vegas is so that's where the actual nucleus of the Vegas nerve is located so the cardiac exhibitory center is connected with the vagus nerve and if you guys remember we said the vagus nerve is primarily a parasympathetic nerve so we can say that the cardiac inhibitory Center is connected with the parasympathetic nervous system okay so let's get this straight then if this comes into this nucleus here what is this blue nucleus here called nucleus of tractus solitarius right once this gets uh sends the gets the signals from the glossop frenal and the vagus nerve it's going to do two things it's going to send signals to the cardiac accelator center it's going to send signals to the cardiac inhibitory Center and it's going to do one more thing and it's going to send signals to the vasom motor Center if our blood pressure is low what are we going to want to do we're going to want to H have the heart contract more or the heart rate to increase so that we can have more blood coming out why because you have to remember this formula I'm going to put smack dab right here in the middle what do we say blood pressure is equal to the cardiac output multiplied by the total peripheral resistance this is so important this formula is so crucial to understand so we're going to have to try to change this up a little bit okay so first thing we're going to do here if we look at this we're going to want to speed up the heart rate and we're going to want to have the heart rate um increased and we're going to want the contractility to increase so we're going to stimulate the cardiac accelator center because if we do that we're going to increase our cardiac output if we increase heart rate because what again what is heart rate equal to remember cardiac output is equal the heart rate times the stroke volume so if you increase the heart rate you increase the cardiac output if you increase the stroke volume you increase the cardiac output you increase the cardiac output you increase the blood pressure so first thing we're going to want to do is we're going to stimulate the cardiac accelator center but we don't want the cardiac inhibitory Center coming into play here because it's going to try to slow the heart rate down so we want to inhibit this Center so stimulate the cardiac exelator inhibit the cardiac inhibitory but then we got to do one more thing we have to stimulate the vasom motor Center because what the vasom motor sensor is going to do is it's going to activate the sympathetic nervous system to increase your total peripheral resistance it's going to constrict the blood vessel how do I know that because you know there's another formula here let's just get rid of the diaphragm we don't need it anyway resistance is equal to 8nl over P R4 this is pel's uh part of the poel equation he says that as your radius decreases as the radius decreases the resistance increases significantly so we're going to constrict the vessels which is going to decrease the radius which is going to increase the resistance and if you increase the resistance you increase the blood pressure okay so now that we know what what centers are being controlled let's see how they're being affected so let's come over here to this side for a second so we can see it a little better so I just had to I drew another card uh central nervous system here and again real quickly this one is cardiac accelator vasomotor center cardiac inhibitory and nucleus of tractus solitarius all right we already said the cardiac exelator center was activated if the cardiac exelator center is activated it'll come down to a specific region in the spinal cord okay this region is right around T1 uh to anywhere from T1 to L2 okay anywhere from T1 to L2 this is the sympathetic outflow so this is the SNS outflow okay sympathetic nervous system outflow particularly most of the fibers come from from T1 to T5 but anyway these cardic accelator fibers come down and they act on these preganglionic fibers in the lateral gry horn these fibers come out and they come to a gangon like a sympathetic chain gangon or a a cervical gangon either way they come to these gangon and then they come out where are they going to go they're going to go to two destinations one destination is it's going to go to a special structure located within the right atrium and another structure which is located near the actual bifera where the actual Atria and the ventricles are separated what are these two areas one of the areas is going to go to What's called the SA node the other area is just going to go to What's called the AV node what is it going to do there let's see what are these chemicals releasing what are these guys releasing under the SA node and the AV node let's look at it right here let's say that this is the SA node or the AV node okay let's say that the SA node or AV node what is it going to try to do okay here is the chemical that it releases it releases what's called noro epinephrine norepinephrine is going to come over here and bind onto these receptors on the SA node or AV node okay now when the norepinephrine binds onto these receptors what kind of receptors are they you know they're called beta 1 adrenergic receptors when it binds onto these beta 1 adrenergic receptors it activates a specific protein one is it activates a g protein particularly G stimulatory protein which gets rid of you guys should know this by now GDP and binds GTP which turns it on this guy will come and activate a effect enzyme that aor enzyme is called Aden cyclas Aden cyclas is going to do what so once it stimulates aen cycl Aden Cycles converts ATP into cyclicamp once it activates cyclic cyclicamp activates protein kinas a and what does protein kinas a do it comes over to the membrane and it finds these special channels located on the membrane look at these channels look at these beautiful beautiful channels here these beautiful channels are specific Al for calcium and what it does is this guy comes over here and it puts a phosphate onto this Channel and when it does that it opens up the channel it activates the channel and calcium ions start flowing in very very excessively and what is this going to do well if it flows into the sa Noe or the AV Noe we're going to have more calcium coming in which is going to ultimately increase the heart rate okay we're going to have more action potential so more calcium coming in allows for more action potentials more action potentials means the increasing heart rate if you increase the heart rate what does that increase come over here for a second we said that whenever you increase the heart rate you increase the cardiac output when you increase the cardiac output you increase the blood pressure that's what it's going to do so it's going to try to increase the heart rate which will do what increase the cardiac output as you increase the cardiac output you increase the BP voila that's one way that we can fix this whole issue so one thing that you're going to notice with someone who is having low blood pressure is that they're going to try to compensate by increasing the heart rate so their heart rate might be a little higher their pulse might be a little higher right okay that's one thing that we're going to know what else can to do these sympathetic nerves they can also let's follow these bad boys here because they can also go to two other destinations they can come over here and they can come to The myocardium of the heart the muscle of the heart because the essay note in the AV node and the peni fibers and the bundle of hiss all that stuff those guys are primarily nodal cells they don't contract cont ract these cells here do contract let's follow this other fiber over here for a second CU it's going to come over here to this myocardium here also okay what is it going to do how is it going to act on this guy it's going to act through the same mechanism so if we were to just clean this up a little bit here say that we clean this up a little bit I'll explain to you what exactly is happening so what happens the only thing that's a little bit different in this situation in this cell is it activates cyclic right and then it will actually activate protein KY a okay protein KY a will still come and phosphorate these channels so this is the same thing except now instead of it acting on the SA node and the AV node it also can act on The myocardium of the heart the contractile unit so this is the contractile unit when it does this calcium flows in as more calcium starts flowing in what happens more calcium means more crossbridge formation if we have more cross Bridges what do I mean by cross Bridges you know you have these things here like um let's say here I have a thin filament I have actin and over here on this part I have the thick filament which is going to be the mein so I have thin filament which is pretty much the consisting of the actin and over here I'm going to have the myosin what happens is if I have more calcium coming to this area it's going to bind onto a protein called troponin which will change the shape of the tropomyosin which will open up these active sites for the myin to bind into acting and Trigger the power stroke initially so what's the overall result if we have more calcium we're going to have more cross Bridges and then more cross Bridges means more a powerful contraction so an increase in contraction now if you guys know anything about contraction if you increase contractility what does that do it increases stroke volume if you increase the stroke volume what does that do let's come over here for a second we said that if you increase the stroke volume you increase the cardiac output you increase the cardiac output you increase the blood pressure okay so so far we've been able to settle two things here so let's just make it nice and clean here and get the overall effect of all of this so that way we know exactly what is happening again we can say the sympathetic nervous system is acting on the SA node AV node and The myocardium of the heart and again it's doing it through this protein kyes a who's coming in phosphor lating these calcium channels calcium is flowing in very heavy and the overall result is to do two things one is to increase the heart rate and the other one is to increase the contractility all right sweet and these are both going to try to increase the blood pressure that's one way that our body's going to deal with that okay what about this vasom motor Center we also said the heat was stimulated right so we said the nucleus subtracted solarius stimulated this guy stimulated this guy and inhibited this guy what does the vasil motor Center do it basically does the kind of the same thing as the actual uh cardiac exelator center he comes down here and he gives off these fibers also so he gives off some fibers and they go to the preganglionic uh neurons located within Thal Lumber region of the spinal cord and they come out okay so these guys come out now they're going to go to a ganglion some type of gangon out here and what they're going to do is they're going to go to the blood vessels they're going to go to the blood vessels so look at this let follow this sucker here if we follow this guy here where is he going to go oh yeah baby there he goes right there okay so what happens activate the mo vasomotor nerve center the vasomotor nerve center brings these postganglionic sympathetic fibers to the blood vessels where in the blood vessels to be very very particular it's particularly located within the Tunica Media that's where these fibers are going to terminate they're going to go to the tunic Comedia the muscular layer of the actual arterials what it's going to do is it's going to bind onto specific receptors in that area Okay so if it wants to contract it it'll primarily act through alpha 1 adrenergic receptors and what chemical is it going to be releasing here it's going to be releasing neuro epinephrine when it releases norepinephrine norepinephrine is going to come in here and it's going to bind onto this receptor when this norepinephrine binds on let's make this nicer let's make it very very pretty we want it to be pury well Norine binds onto this alpha 1 adrenergic receptor what happens he basically Works through a special mechanism and this mechanism that he's going to try to exert is he's going to try to stimulate this adrenergic receptor to cause the smooth muscle cell to contract it's going to try to bring more calcium into the smooth muscle cells if that happens and this this actual smooth muscle contracts what is it going to do to the blood vessel it's going to try to constrict the blood vessel so what is this going to result in it's going to result in Vaso constriction so now what is it going to do if you Vaso constrict the blood vessel you're going to squeeze the blood vessel and that's going to decrease the diameter well if you decrease the diameter of the blood vessel what's that going to do the radius what's half of the diameter the radius so now I'm going to decrease the radius of the blood vessel if I decrease the radius of the blood vessel what did we say we said pel's equation is that whenever you decrease the radius you increase the resistance by four folds that's significant so I'm going to increase my total peripheral resistance and what do we say if you increase total peripheral resistance it increases your blood pressure so as a result you're going to have an increase in the BP and voila another way to try to fix the problem okay so there's another way that we're trying to fix the problem so one way is that we try to do so far is increase the heart rate and increase the contractility the other way is to constrict the blood vessel to increase the resistance to try to bring up the BP okay that's one way okay now that's that for the heart aspect but we want to see everything connected because that's what you want to understand how things are connected so now what we got to do is actually we have to see one more thing for the heart I actually deled we need one more thing you know the heart has other sympathetic fibers here too it has other sympathetic fibers and these sympathetic fibers are very very special because what happens is these sympathetic fibers they actually they shouldn't terminate here there should be some special sympathetic fibers that will actually pass right through the sympathetic Chang ganglia and when they pass through the sympathetic Chang ganglia they actually syapse on the cell bodies of the postganglionic motor neurons within the Adrenal medulla and you know what the Adrenal medulla consists of it consists of these chromin cells and these chromin cells consist of postganglionic motor neurons and guess what they release they release two chemicals one is epinephrine so one is they release Epi the other one is they release neuro epinephrine but which one of they releasing a larger amount they're releasing 80% epinephrine and about 20% of it in norepinephrine what can epinephrine do it can do the same thing norepinephrine did it can come over here and cause vasil contri in the blood vessel it can act on The myocardium of the heart and cause increased contractility it can even act on the SA node and the AV node and increase the heart rate so it can do all of those things also okay okay so just so that we're aware this is another mechanism here that we try to utilize to increase the actual uh systemic response to increase our blood pressure all right sweet that's that part let's go on to the next thing then okay so let's see how the actual kidneys are involved in this let's see how the kidneys are involved so here we have a kidney the kidneys are very very uh specific and the reason why is they have they have their own Auto regulation mechanism because you have to protect your kidneys whenever there's certain types of system make changes in your blood pressure but one thing that the kidneys do to protect themselves let's say that I have low BP right again so low blood pressure low systemic blood pressure coming in and there's going to be less blood coming from the actual vessels into the kidney right less blood coming into the actual kidney now whenever there is low BP there's special cells in the kidney that pick up that low BP these cells are called the JG cells these JG cells respond to that decrease in BP and they release a chemical called renin they release a very very important chemical here called renin now what is it about renin that's going to help us out oh you'll see so now what we're going to do is the kidney is going to release this renin out into the bloodstream okay so renin is going to released be released out into the bloodstream so what happened low BP activated these JG cells to cause them to produce renin you know what else is really crazy remember that epinephrine epinephrine that was also released it can come over here and it can act on beta 1 adrenergic receptors on the JG cells of the kidney and also increase the production of renin so two things are acting to increase the production of Rena one is low BP and the other one is the actual production of epinephrine which can act on the beta 1 adrenergic receptors and Trigger the release of renin what's renin going to do okay let's follow renin renon comes out into the circulation and as he's coming through the circulation he runs into another protein okay because renin is kind of like a nice enzyme the liver produces a really cool protein this protein that the liver is producing and it's constantly circulating throughout the bloodstream is called angio tensen tensin gen what happens is renin is going to come and cleave angiotensinogen so angiotensinogen is kind of an inactive uh protein what happens is renin is going to act as an enzyme and it's going to cut certain amino acids off angiotensinogen when it cuts certain amino acids off of angiotensinogen it does something really special it converts angiotensinogen into another molecule this molecule is called Angiotensin one so what is this molecule called again the molecule that it actually produces is called Angiotensin one so as a result when angot tensen gets converted into Angiotensin one look what happens here now we have Angiotensin one now Angiotensin one is still not good enough to produce this systemic effect that we're looking for so what happens Angiotensin one he continues throughout the actual blood Pro process right so let's say he goes into the actual right atrium from the right atrium he gets pumped into the right ventricle from the right ventricle he gets pumped up into the pulmonary trunk through the pulmonary arteries and he gets over here into the pulmonary capillaries in the actual lungs in the lungs there's another special enzyme this enzyme is called Angiotensin converting enzyme we also like to denote it as Ace Angiotensin converting enzyme this enzyme will act on Angiotensin one so what's going to be present right here at this point in time right here we're going to have this still kind of precursor molecule called Angiotensin one what happens is Ace is going to act on Angiotensin one and convert Angiotensin one into a very powerful hormone called Angiotensin 2 okay and Ace is going to drive this process so Ace andot tens converting enzyme is stimulating Angiotensin one to go into Angiotensin 2 now where does Angiotensin 2 go oh he's got some destinations this guy he does so much okay so let's see all the things that Angiotensin 2 is doing first thing it's going to come over here to the adrenal cortex you know in the adrenal cortex we have these cells called Zona glomerulosa so it's called the Zona glosa cells this Angiotensin 2 will come over here and he will act on special receptors on the Zona glosa stimulate the Zona glosa cells to release a chemical into the bloodstream and this is a very very powerful hormone this hormone is called aldosterone so this is called aldrum we're going to see what he does in a second because I'm going to combine him with another hormone that Angiotensin 2 also stimulates so look here Angiotensin 2's done that so far he also comes down a little bit more he's like hey you know what I see someone else that I like and he comes through the circulation into the actual part of the brain the central nervous system you know what this structure is called This is called the hypothalamus this right here this top part here is the hypothalamus this part down here from this region to this region is called the pituitary gland so it's specifically called the pituitary gland you know specifically this is the posterior pituitary and this is the anterior pituitary okay to together they make up the entire pituitary gland or the hypothesis as you can call it okay so there is that what happens is angiotensin two comes over here and he acts on specific receptors inside of the hypothalamus you know there's a special nucleus here this kind of group of nuclei right here this group of nuclei here is called the Supra optic nucleus what happens is Angiotensin 2 comes over and stimulates the super optic nucleus when the super optic nucleus is activated it sends Action potentials down the axons the tract the hypothalamic hypophysial tract as it does that it triggers the release of a special chemical called anti dtic hormone also you can call it vasopressin so what does it release into the bloodstream then it also releases ADH into the bloodstream so now we have two things that it's triggered one thing is it's triggered the production of ADH the other thing is triggered the production of Ostrum but guess what he's like I'm not done he's going to do something else he says I see some other neurons over here that appealing are appealing to me these neurons control your thirst so there's other neurons that are are located within the hypothalamus that control your thirst Angiotensin 2 comes over and stimulates the hypothalamic thirst centers and this triggers the release of certain chemicals that're going to bring about the actual desire for thirst so if you drink more water let's say you become thirsty so there's an increase in your thirst what are you going to do you're going to takeing more water if you or fluids whatever you're going to bring in more water so increase absorption of fluids across the git if you have more absorption of fluids then what's going to happen your blood volume is going to go up you know blood volume actually increases a specific thing called the end diastolic volume we talked about that in cardiac output what happens is in diastolic volume if that increases that increases your stroke volume if you increase stroke volume increase cardiac output and if you increase cardiac output you increase BP so that's another way that we're dealing with it so one way we dealt with it is by increasing thirst and by producing adstone and ADH what in the heck do these guys do let's see let's follow ADH and ostrin over here to the kidney okay what I'm doing is I'm taking a the structural and functional unit out of the kidney so you see here in the kidney we have the kidney I'm taking out a special structure called the nephron okay so I'm looking at What's called the nefron so I'm looking here specifically let's actually put it right here because we're not going to use too much of this right here we're looking at a special structure called the nefron what happens is ADH and OST are going to act in two different parts here ADH is going to act in What's called the collecting duct okay there's actually what's called V2 receptors and what happens is ADH also known as vasopressin comes over here and acts onto this receptor when ADH acts onto this receptor he activates a g stimulatory protein which you guys already know the story activates a denate cyclas which converts ATP into cyclic cyclic increases the protein cyas a levels and if this happens remember those special proteins oo let's use the teal we have those special proteins remember we had the vesicles here with those special aquaporin these guys are special proteins called aquaporin two what happens is protein kyes a comes over here and phosphorites this uh these vesicles which triggers this process of bringing those actual channels towards the membrane so this vesicle fuses with the membrane and what it does is it puts these channels into the membrane so now look we have another channel here let's say that we put three channels in okay so what did protein KY a do protein cye a phosphorilated these vesicles which are containing this protein called o aquaporn 2 as it did that so now let's get this aquaporn 2 out the way here cuz we phosphorated the aquaporn 2 it was actually presynthesized in the cell right but ADH can also increase the synthesis of him so what we did is we have protein kyes a phosphorate this vesicle here containing all these aquaporn 2 molecules now that he did that and he phosphorated this guy he stimulated it by phosphor it we put these actual channels into the membrane as we do that what's flowing through the actual kidney tubules what's pretty much most of your urine made up of it's actually 93% water so what happens is water flows through these actual aquaporin what type again aquaporin type two then what happens is they come out of these aquaporin twos and they move into your circulation so let's say that I actually draw here a part of your actual circulation actually no it's right here let's just bring it over here there's your circulation right there let's see that this actually moves over here and we bring the water into the circulation if you increase the volume of water inside of the actual blood you're increasing the blood plasma if you increase the blood plasma you increase the actual what blood volume if you increase the blood volume you increase the edv if you increase the edv you increase the stroke volume increase the stroke volume increase the cardiac output you increase the cardiac output you increase the blood pressure okay holy crap now what is aldosterone doing aldosterone is actually coming over here and it's acting on this specific area here called the distal convoluted tubal and again the ADH was acting on a specific area called the collecting duct but it can also act on the distal convoluted tubal aldosterone is a steroid hormone so he comes in let's say here's the nucleus of the cell aldosterone comes in and binds onto a special intracellular receptor so let's say here I have an intracellular receptor okay Ostrum will come over here and he'll bind onto this intracellular receptor when he does that this receptor steroid hormone receptor interaction will come over activate specific genes when it activates genes it'll produce three main proteins okay one protein here one protein here and I'll put one protein back here the main one that it's going to put out here is going to be uh uh a protein for sodium channels okay so it's going to put a protein there for sodium channels it's also going to put a protein back here in the basolateral membrane and it'll prod put one more protein into the membrane here which is going to be for potassium so what is it going to do if it does this this potassium channel will allow for potassiums to leak out this sodium channel right here will allow for sodium ions to come from the filtrate into the cell and then eventually into the blood and then what happens is we have this pump back here which is doing uh doing what it's pumping three sodium ions out of the cell and it's pumping two potassium ions into the cell utilizing ATP okay what's the whole purpose of this we're taking the protons from the blood if your proton levels are really high we're getting rid of those protons we're excreting out the protons and we're bringing in sodium if sodium starts actually moving into the blood so let's say that sodium is moving into the blood here's your sodium ions it's moving into the blood who else likes to follow water but remember what hormone has to be present in order for water to be able to get absorbed here ADH so ADH would have to act on V2 receptors and then V2 receptors would increase the cyclic pathway and increase the expression of aquaporin type two and who would follow the sodium the water okay and then water if the water is going into the blood what happens again if you increase the water volume inside your bloodstream you increase the blood plasma if you increase the blood plasma volume you increase the blood volume if you increase the blood volume you increase the edv which is the end diastolic volume if you increase that you increase the stroke volume if you increase the stroke volume you increase cardiac output and then increase blood pressure holy crap okay we did that too one other thing I'm going to mention very very briefly is that angiotensin two can also act on what's called the proximal convoluted tubal cells so Angiotensin 2 also has receptors here that he can bind to and trigger an increase in what's called sodium reabsorption chloride reabsorption and water reabsorption if I bring into the bloodstream all three of these chemicals primarily that of increase water and increase in sodium and increase in chloride what's going to happen increase the blood volume increase the indiy volume increase the stroke volume increase cardiac output blood pressure you get the deal that's that part okay now another thing Angiotensin 2 also has receptors present on the arterials just like the epinephrine does so what else could Angiotensin 2 do besides stimulating ostrin production besides stimulating ADH it could also come over here and bind onto these receptors these d tensin 2 receptors which are located on the tunic media right of the arterials so what is this guy right here going to be this is for the Tunica Media just like the sympathetic nervous system when it does that it actually causes Vaso constriction if you cause that whole vasal constrictive process we already know what it's going to do it's going to increase your blood pressure okay how if you vasal constrict the blood vessels you decrease the diameter of the blood vessels you decrease the radius of the blood vessels using pel's equation that increases the resistance significantly which increases the blood pressure okay that's that part another thing that actually happens in the kidneys is if you think about it what did we say was happening to the blood flow going to the kidneys there was a very low blood flow going to the kidneys if there's low blood pressure right you're going to have very little blood going into the kidneys that means that you're going to have what kind of urine output as a result here you're GNA have a decrease in urine output so as a result you're also going to have decrease urine output why is that significant because if you have a decreased urine output what that's going to try to do is it's going to try to decrease the amount of volume of of uh fluids that are being lost in the urine so that we can maintain the actual volume within the blood to maintain our blood pressure so we're going to want to decrease the urine output okay and this is because if you have low blood pressure it leads to what's called a low glomular filtration rate we talk about this in the kidneys and if you have a low Glam filtration rate you're going to have a decrease urine output what do you call that whenever you decrease urine output oi Gia okay okay and again by doing that you conserve a lot more volume you don't leak as much volume out in the urine one other thing that can affect our actual blood pressure is um talk about a little bit more later but we also have the actual cortex the cortex also has influence on the actual medular respiratory centers the hypothalamus which is located right here right so you know that you have the hypothalamus right here the hypothalamus also has the ability to control your blood pressure you also have special nuclei in this area what are these nuclei here called special nuclei called limic nuclei and these can also influence the actual respiratory centers so because of that you have in certain situations like maybe in stress or emotions or anxiety certain things like that that can actually influence these centers within the brain by what way maybe increasing the cardiac accelator center if you're really really stressed if you're really really anxious you probably noted that your heart is racing a lot you're having increased contractility maybe palpitations and the reason why is because lyic nuclei hypothalamus and even some of the actual cerebral cortex has a little bit of influence on the uh medular cardiovascular and vasom motor centers all right Engineers so in this video we covered a lot of information about what our body does in certain situations like in hypotension or low blood pressure and how it tries to regulate that I hope all of it made sense I truly do I hope you guys enjoyed it um in the next video we're going to talk about what happens how what are the compensation mechanisms whenever our blood pressure is too high so then we'll get to see exactly what this cell was used for which is going to be how acetylcholine works on these SA node cells and AV node cells and we'll see other different effects with the kidneys and other different types of organs all right I hope to see you guys there and uh as always until next time