Cardiovascular | Blood Pressure Regulation | Hypotension

I'm engineers 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 various different causes and how that again how our body can compensate for that to bring our blood pressure back up okay so what would actually trigger this to happen okay we said low blood pressure but let's get a little bit more specific okay what are we actually considered 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 that when whenever your systolic blood pressure okay the actual ventricular pressure the amount that your ventricles are trying to expel specifically the left out of the hardening to the great vessels whenever it is less than a hundred millimeters of mercury so whenever your systolic blood pressure is less than a hundred millimeters 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 millimeters of mercury it may be even significantly lower maybe down to like 80 millimeters of mercury okay in certain situations where I can get really low like in hypovolemic shock so talk about all these different mechanisms okay well first off how does our body detect this changes in blood pressure through baroreceptors pressure receptors where can you find those little suckers you're going to find them right over here we talked about these guys threw out a series of our videos right and we know that we're going to have these special types of baroreceptors 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 baroreceptors and they have these sensory afferent nerve endings here and these sensory afferent nerve endings are again they're going to be located within in this area they or 'dick sinus so again what were these guys here called they're called Barrow receptors and they're located in a or tick sinus okay now these baroreceptors are very specific and the reason why is these Bayer receptors that are actually taking this information and detecting the changes in the blood pressure this one located within the ORD of sinus is carried on a specific cranial nerve and that cranial nerve is cranial nerve 10 which is also called the vagus nerve so this is a ferrant fibers general visceral efferent 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 carotid artery so this one here is called the left common carotid 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 carotid artery right right at that bifurcation point you're going to notice there is actually going to be some bear receptors located within what's called the carotid sinus so what does these ones right here called these right here are your baroreceptors in carotid 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 afferent nerve endings that are actually with connected as the bear acceptors on the carotid sinus this sensory afferent information is carried on cranial nerve nine which is the glossopharyngeal nerve okay so the aortic sinus has bare receptors which we carry on the sensory afferent fibers of vagus the Bayer receptors in the carotid sinus are going to be carried on the sensory afferent fibers of the glossopharyngeal nerve or cranial nerve nine 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 baroreceptors respond to change in 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 axon right or in this case this part here is the peripheral process this is the sensory nerve ending 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 Bair receptors which opens up these channels on the bare acceptors sensory nerve endings 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 a hundred millimeters of mercury maybe even very significant about 80 is that going to be stretching the blood vessel walls no if it doesn't stretch the blood vessel walls is there going to open up these channels no it's 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 AP's 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 structure on the blood vessel wall is pretty much we can say not going to stimulate the vagus nerve so we like to say it as though it's really inhibiting the nerve okay it's inhibiting the sensory afferent fibers of the vagus nerve it's also inhibiting the sensory afferent fibers of the Bair receptors that are located within the carotid sinus carried on the also fringe owner when they take this information up to the nucleus of tractus solitarius the nucleus of tractus solitarius kind of sift through that information as it sits 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 excel at Ori sent I'm going to put that a CA the cardiac accelerator this Center is connected with our sympathetic nervous system so the cardiac accelerator nerves connected with your sympathetic nervous system this brown one here is called the vaso motor center I'm going to the VM the vasomotor center and the vasomotor 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 that's where the actual nucleus of the vagus nerve is located so the cardiac exhibitory center is connected with the vagus nerve and 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 down if this comes into this nucleus here what is this blue nucleus they're called nuclear subtractive solitarius right once this gets sense this is getting signals from the glossopharyngeal in the vagus nerve it's going to do two things it's going to send signals to the cardiac cell Tory Center it's going to send signals to the cardiac inhibitory center and it's going to do one more thing that's going to send signals to the vasomotor center if our blood pressure is low what are we going to want to do we're going to want to have the heart contract more the heart rate to increase so we can have more blood coming out why because you have to remember this one 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 have the heart rate increase and we're going to onto current contractility to increase so we're going to stimulate the cardiac accelerator 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 to 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 accelerator but we don't want the cardiac inhibitory set are coming into player because it's going to try to slow the heart rate down so we want to inhibit this center so stimulate the cardiac accel Tory inhibit the cardiac inhibitory but then we got to do one more thing we have to stimulate the vasomotor center because what the vasomotor center 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 8 and L over PI R for Isis police cells part of the PI cells 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 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 car do a central nervous system here and again real quickly this one is cardiac Excel Tori basil Motor Centre cardiac inhibitory and nucleus of tractus solitarius all right we already said the cardiac accelerator was activated if the cardiac accelerators activated it will come down to a specific region in the spinal cord okay this region is right around t1 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 t 1 to t 5 but anyway these cardiac Castellitto fibers come down and they act on these preganglionic fibers in the latter of gray horn these fibers come out and they come to a ganglion like a sympathetic chain ganglion or a cervical ganglion either way they come to these ganglion 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 bifurcation 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 D s a node the other area is it's going to go to what's called the a V node what is it going to do there let's see what do these chemicals releasing what are these guys releasing onto the SA node an 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 our AV node what is it going to try to do okay here is the chemical that it releases it releases what's called Norrell 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 on to these beta-1 adrenergic receptors activate 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 effector enzyme that effector enzyme is called adenylate cyclase adenylate cyclase is going to do what so once it stimulates adenylyl cyclase adenylate cyclase converts ATP into cyclic a MP once it activates the co2 MP cyclic GMP activates protein kinase a and what does protein kinase a do it 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 specifically 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 in calcium mine start flowing in very very excessively and what is this going to do well if it flows into the SA node to the AV node 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 potentials so more calcium coming in allows for more action potentials more action potentials means an increasing heart rate if you increase the heart rate what does that increase come over here for a second we said that when you increase the heart rate you increase the cardiac output when you increase the cardiac output you increase the blood pressure that's what's going to do so it's gonna try to increase the heart rate which will do what increase the cardiac output as you increase the credit output you increase the BP wallah 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 I'm going to know what else can I 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 SA node in the AV node and the Purkinje fibers and the bundle of his-- all that stuff those guys are primarily nodal cells it'll contract these cells here do contract let's follow this other fiber over here for a second cause 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 actually 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 a and P right and then it will actually activate protein kinase a okay protein kinase a will still comment phosphorylate these channels so this is the same thing except now instead of acting on an SA node and AV node it also can act on the myocardium of the heart the contractile unit so this is a contractile unit when it does this calcium flows in as more calcium starts flowing in what happens more calcium means more cross bridge formation if we have more cross bridges what do I mean by cross bridges you know you have these things here like um I'd say here I have the thin film and I have actin and over here on this part I have the thick filament which is going to be the myosin so if 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 myosin to bind into acting and trigger the powerstroke 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 powerful contraction so an increase in contraction now as 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 a nice and clean here and get the overall effect of all of this that way we know exactly what is happening again we can say the sympathetic nervous system is acting an SA node AV node and the myocardium of the heart and again it's doing it through this protein kinase a who's coming in phosphorylating these calcium channels calcium is flowing and 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 vasomotor Center we also said that he was stimulated right so we said the nucleus of tractus solitarius stimulated this guy stimulated this guy and inhibited this guy what does the base of motor center do it basically does the kind of the same thing as the actual cardiac accel Tory Center he comes down here and he gives off these fibers also so he gives off some fibers and they go to the preganglionic neurons located with them for a Colombo reach in 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 ganglion 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 with all of this sucker here if we follow this guy here where is he gonna go oh yeah baby there he goes right there okay so what happens activate the modes of basal motor nerve center the vasomotor nerve center brings these postganglionic sympathetic fibers to the blood vessels wherein the blood vessels can 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 tunica media the muscular layer of the actual our arterioles 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'll primarily act through alpha one adrenergic receptors and what chemicals are going to be releasing here it's going to be releasing Norrell 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 make it very very pretty we wanted to be purring when norepinephrine binds on to this alpha one a generic 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 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 vaso constriction so now what is it going to do a penis days will 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 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 do we say we said poi sales equation is that whenever you decrease the radius you increase the resistance by fourfold that's significant so I'm going to increase my total peripheral resistance and what do we say if you're increased 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 that we try to do so far is increase the heart rate 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 we want to see everything connected because that's what you want to understand how things are connected so now we got to do is actually have to see one more thing for the heart I actually delight we need one more thing you know the heart has all the sympathetic fibers here too and has other sympathetic fibers and these sympathetic fibers are very very special because what happens is these sympathetic fibers they're actually they shouldn't terminate here there should be some special sympathetic fibers that will actually pass right through the sympathetic chain ganglia and when they pass through the sympathetic chain ganglia they actually sign apps on the cell bodies of the postganglionic motor neurons within the adrenal medulla and what the adrenal medulla consists of it consists of these chromaffin cells and these chromaffin cells consist of postganglionic motor neurons and guess what they release they released two chemicals one is epinephrine so one is they release epi the other one is they release norepinephrine but which one of the releasing a larger amount they're releasing 80% epinephrine and about 20 % of it in norepinephrine looking at the nephron do it can do this same thing norepinephrine did it can come over here and cause Bay's a contract and blood vessel it can act on the myocardium of the heart and cause increased contractility it can even act on the SA node in the AV node it increase the heart rate so we can do all of those things also okay so just so that we're aware this is another mechanism here that we try to utilize to increase the actual a systemic response to increase our blood pressure alright 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 see how the kidneys are involved so here we have a kidney the kidneys are very very specific and the reason why is they have they have their own auto regulation mechanism because you have to protect your kidneys whenever there are certain types of systemic 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 are 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 random that's going to help us out all 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 rennet is going to really be released out into the bloodstream so what happened low BP activated these JG cells to cause them to produce renin you know health 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 increased the production of renin so two things are acting to increase the production of rhythm 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 Ranen going to do okay let's follow Renan rainin comes out into the circulation and as he's coming through the circulation he runs into another protein okay because written kind of like a nice enzyme the liver produces a really cool protein this protein that the liver is producing it's constantly circulating throughout the bloodstream is called angiotensinogen can send o j-- in what happens is Renan is going to come and cleave angiotensinogen so angiotensinogen is kind of an inactive protein what happens is Renan 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 angiotensinogen gets converted to angiotensin one look what happens here now we have angiotensin 1 now angiotensin 1 is still not good enough to produce this systemic effect that we're looking for so what happens angiotensin 1 he continues throughout the actual blood 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 1 so what's going to be present right here at this point right here we're going to have this still kind of precursor molecule called angiotensin 1 what happens is ace is going to act on angiotensin 1 and convert angiotensin 1 into a very powerful hormone called angiotensin 2 ok and ace is going to drive this process so ace angiotensin converting enzyme is stimulating intense and one to go into angiotensin 2 now where does angiotensin 2 go well he's got some destinations this guy he does so much ok 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 glomerulosa cells this angiotensin 2 will come over here and he will act on special receptors on the zona glomerulosa stimulate the zona glomerulosa cells to release a chemical into the bloodstream and this is a very very powerful hormone this hormone is called aldosterone so this woman is called aldosterone we're going to see what he does in a second because I'm going to combine him with another hormone that angiotensin ii also statements so look here angiotensin 2 has done that so far he also comes down a little more he's okay you know 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 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 ok took together to make up the entire pituitary gland or the hypothesis as you can call it ok so there is that what happens is angiotensin 2 comes over here and he acts on specific receptors inside of the hypothalamus here is a special nucleus here this kind of group of nuclei right here this group with nuclei here is called the Supra optic nucleus what happens is angiotensin ii comes over and stimulates the super optic nucleus when the super optic nucleus is activated it sends action potentials down the axons attract the hypothalamic hypophyseal tract as it does that it triggers the release of a special chemical called antidiuretic hormone also you can call vasopressin so what is it released into the bloodstream then it also releases ADH into the bloodstream so now we have two things that is triggered one thing is this triggered the production of ADH the other thing that's triggered the production of aldosterone 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 appeal and are appealing to me these neurons control your thirst so there's other neurons that are located within the hypothalamus that control your thirst angiotensin ii comes over and starless the hypothalamic thirst centers and this triggers the release of certain chemicals they're going to bring about the actual desire for thirst so if you drink more water let's did you become thirsty so there's an increase in your thirst what are you gonna do we're going to take in more water if you or fluids whatever you're going to bring in more water so increased absorption of fluids across the GI t if you have more absorption of fluid 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 and cardiac output what happens is in diastolic volume and that increases that increases your stroke volume if you increase stroke volume increase clinic 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 deal with it is by increasing thirst and by producing a lobster and an 88 what in the heck do these guys do let's see let's follow ADH and a - run over here to the kidney okay what I'm doing is I'm taking a us the structural and functional unit out of the kidney so you see here in the kidney we have the kidney I'm taking on a special structure called the nephron okay so I'm looking at what's called the nephron 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 nephron what happens is ad hoc 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 on to this receptor when ADH acts on to this receptor he activates a G stimulatory protein which you guys argue know the story activates adenylate cyclase which converts ATP into cyclic AMP e cyclic GMP increases the protein kinase a levels and if this happens remember those special proteins let's use the teal we have those special proteins where we had the vesicles here with those special aquaporins these guys are special proteins called aquaporins - what happens is protein kinase a comes over here and phosphorylates this 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 put 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 a protein kinase they do protein kinase a phosphorylated these vesicles which are containing this protein called aquaporin - as it did that so now let's get this aquaporin 2 out of the way here because we phosphorylate the aquaporin - it was actually pre synthesized in this cell right but ADH can also increase the synthesis of him so what we did is we have protein kinase a phosphorylate this vesicle here containing all these aquaporin two molecules now that he did that and he phosphorylated this guy he stimulated by phosphorylating 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 a made up of it's actually 93% water so what happens is water flows through these actual aquaporins what type again aquaporin type two then what happens is they come out of these aquaporin tubes and they move into your circulation so let's say that I actually draw here a part of your actual circulation actually notes right here let's just bring it over here there's your circulation right there let's say 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 increase the edv if you increase the edv increase the stroke volume increase to stroke point increase the cardiac output you increase the cardiac output you increase the blood pressure okay holy crap now what is our doctrine doing I'll dodge thrown it's actually coming over here and it's acting on this specific area here called the distal convoluted tubules and again the ADH was acting on a specific area called the collecting duct but it can also act on the distal convoluted tubule aldosterone is a steroid hormone so he comes in let's say here's the nucleus of the cell aldosterone comes in and binds on to a special intra cellular receptor so let's say I have an intracellular receptor okay aldosterone will come over here and help bind on to this intracellular receptor when he does that this receptor steroid hormone receptor interaction will come over activate specific genes we have activate genes it will produce three main proteins okay one protein here one protein here and I'll put one protein back here the main one that is going to put out here is going to be a protein for sodium channels okay so it's going to protein there for sodium channels it's also going to put a protein back here in the basolateral membrane and it will produce 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 potassium eyes to leak out this sodium channel right here will offer 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 doing what its 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 or 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 V two receptors and then V two receptors would increase the cyclic AMP P 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 of your bloodstream you increase the blood plasma if you increase the blood plasma volume increase the blood volume if you increase the blood volume increase to e DV which is the end diastolic volume if you increase that you increase the stroke volume if you increase the stroke volume 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 ii can also act on what's called the proximal convoluted tubule cells so angiotensin ii also has receptors here that he can bind to and trigger an increase in what's called sodium reabsorption chloride reabsorption and and water re-absorption if I bring into the bloodstream all three of these chemicals primarily that of increased water and increase in sodium and increase in chloride what's going to happen increase the blood volume increase the indus valley volume increase the stroke line 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 arterioles just like the epinephrine does so what else could angiotensin 2 do besides stimulating a bass drum production besides stimulating ADH it can also come over here and bind onto these receptors these danger attention to receptors which are located on the tunica media right of the arterioles so what does 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 vasoconstriction if you cause that whole vasoconstrictive process we already know what it's going to do it's going to increase your blood pressure okay how if you guys will constrict the blood vessels you decrease the diameter of the blood vessels you decrease the radius of the blood vessels using ploy cells 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 a Larry 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 going to have a decrease in urine output so as a result you're also going to have decreased 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 fluids that are being lost in the urine so 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 pressure at least without a lobe lamellar filtration rate we talked about this in the kidneys and if you have a low glomerular filtration rate you're going to have a decrease urine output what do you call it when I did a decrease you're an output Olli urea okay okay and again by doing that you can serve 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 talked about a little bit more later but we also have the actual cortex the cortex also has influence on the actual module a our 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 do these nuclei here called special nuclei called limbic 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 there are certain things like that that can actually influence these centers within the brain by what way maybe increasing the cardiac xcellent or Center if you're really really stressed if you're really really anxious you probably notice that your heart is racing a lot you're having increased contractility maybe palpitations and the reason why is because limbic nuclei hypothalamus and even some of the actual cerebral cortex has a little bit of influence on the medullary cardiovascular and vasomotor centers iein is there 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 that made sense I truly do I hope you guys enjoyed it in the next video we're going to talk about what happened to all the what are the compensation mechanisms whenever our blood pressure is too high so then we'll get to see exactly what this cell is used for which is going to be how acetylcholine works on these SA node cells an AV node cells and we'll see other different effects with the kidneys and other different types of organs einige nerves I hope to see you guys there and as always until next time

Channel: Ninja Nerd

Views: 535,261

Keywords: hypotension, Blood pressure regulation, blood pressure physiology

Id: Yyz0E5CpCNQ

Length: 42min 2sec (2522 seconds)

Published: Tue Aug 01 2017