Cardiovascular | Blood Pressure Regulation | Hypertension

I'm in Jersey this video we're going to talk about what happens whenever your blood pressure is too high if you guys haven't already please go and watch the video on what happens whenever your blood pressure is too low the reason why is that this video is just going to build on top of that so watching that video before is going to give you a very firm foundation before you guys come and watch this video ok so again what we're going to talk about in this video is how the body is going to develop these compensation mechanisms whenever our blood pressure is going to be too high so let's go ahead and get started on that first off what do we call high blood pressure we call it hypertension okay so we call high blood pressure we refer to as hyper tension now hypertension we can really say is whenever the actual systolic blood pressure is greater than a hundred and forty millimeters of mercury and we can also consider it to be hypertension whenever the diastolic blood pressure is greater than 90 millimeters of mercury okay normally we like to be 120 over 80 but whenever the systolic blood pressure is greater than 140 or greater than 90 we consider to be hypertension so for example greater than 140 you have what's called systolic hypertension if the diastolic blood pressure is greater than 90 millimeters of mercury you have what's called diastolic hypertension okay now let's go ahead and mainly mainly focus here on just what happens when I didn't going to get into all the depths of that because I can start getting really confusing let's just say again the blood pressure in general is too high okay that's it we're just going to say that the blood pressure is too high again what are the structures in our body that are responding to these changes in the pressure the blood pressure if you guys remember they were called the baroreceptors and we had two types we had the baroreceptors which are located right at this bifurcation point remember I'm going to kind of denoted here common carotid artery and then it splits into an external rotted artery and an internal carotid artery right so we have two parts here we're gonna have an internal carotid artery which is going to be a branch and then we'll have what's called an external carotid artery which is another branch right at this bifurcation point you have a bunch of these baroreceptors which are located within the carotid sinus also here's your aortic arch on the aortic arch you're also going to have a bunch of Bair receptors that are located within this sinus which is called the aortic sinus so again what are these guys here called they're called your barrel receptors these are the Bair receptors located in the aortic sinus these are the Bair receptors that are located within the carotid sinus now just because we've already talked about it in the other video on low blood pressure what is these cranial nerves here the cranial nerve that's located within the aortic sinus the sensory nerve endings is going to be that for cranial nerve 10 and then the sensory nerve endings that are going to be here within the carotid sinus is going to be for that of cranial nerve nine we also call cranial there are nine the glossopharyngeal nerve cranial nerve 10 the vagus nerve now these guys are going to respond to changes in the blood pressure and I'm going to show you the exact mechanism like we saw in the other video on low blood pressure but what happens is these guys feed information to a special nucleus located within the medulla this nucleus is called the nucleus of tractus solitarius okay I'm gonna denote of NPs now first off we're going to try to stimulate these bad boys we're going to try to stimulate the bear receptors that are located within the aortic sinus and we're going to try to stimulate the bear acceptors located within the carotid sinus but how do we do that let me zoom in on one of the actual sensory afferent nerve endings here okay remember I told you that whenever the blood pressure is too high what's it going to do to the actual blood vessel walls it's going to exert a force on the blood vessel walls and stretch the blood vessel walls when it stretches the blood vessel walls it activates these special channels these special channels on the actual sensory nerve endings member when these channels are activated due to stretch it's going to bring sodium ions into the sensory afferent nerve endings as the sodium starts flowing into the sensory afferent nerve endings what starts happening to the inside of the sensory afferent nerve ending it starts becoming very positively charged as it starts becoming positively charged it develops the depolarization and then the depolarization is going to lead to action potentials okay so what's going to happen here increased stretch you to increase blood pressure activates the sodium channels on the sensory or afferent nerve endings allows for sodium to flow in depolarizes the actual efferent fibers and then sends action potentials down creating their 10 and cranial nerve nine into the central nervous system specifically to the medulla where the nucleus of tractus solitarius is okay now at this point it's going to send signals to three different centers within the medulla okay if you guys remember we said that this red center here is going to be the cardiac extent or center okay then we said that this brown center is going to be the vasomotor center okay we denoted it v m right so vasomotor center but i want to say something else about the vasomotor center there's actually in the vasomotor scintilla stay here we have the actual whole nucleus in the vasomotor center is actually two nuclei there two areas that are really important one is called the c1 area and the other one is called the a1 area now c1 is specifically for constriction of the vessels so this one is mainly for the constriction okay you can kind of member that by see there's a C in the C one and C in constriction so constriction the a1 is 4 vaso dilation I like to remember that there's an A in vasodilation an a1 area okay so really if you guys watch the video on what happens whenever is low blood pressure the low blood pressure stimulated the C one area of the vasomotor center in this situation it's going to inhibit it it's going to inhibit the see one area and stimulate the a one area okay so that's kind of what happens here so really we say before the vasomotor Center was being a stimulative and low blood pressure and high blood pressure it's going to be inhibited but really if we want to be super particularly tuned debiting to see one area and stimulating the a one area whereas in low blood pressure it was stimulating the see one area and inhibiting the a one area okay alright enough of that now if the blood pressure is high we want to stimulate the cardiac cell Tory Center no because it's going to increase the heart rate increase the cardiac output which is going to increase the blood pressure even more you know frekin wait we don't want to do that so we're gonna want to inhibit this guy okay closing hit with the cardiac Excel Tory Center next thing what's this green Center called this Green Center is called the cardiac inhibitory center remember we said that this cardiac inhibitory center is connected with the parasympathetic nervous system if you remember I said the cardiac inhibitory Center is pretty much a part of what's called the dorsal nucleus of Vegas the parasympathetic fibers of the vagus nerve this guy is a part of the parasympathetic nervous system cardiac cell Tori's are part of the sympathetic nervous system you would want to activate the parasympathetic why because the parasympathetic is going to slow down the heart rate okay so what am I going to want to do to this Center I am going to want to stimulate the actual cardiac inhibitory center okay let's see how all of this is going to be affected then so first off if I inhibit let's say here with my cardiac right here this one right here I'm coming down here remember it went down to about the t12 l2 region activated these preganglionic fibers that went out to a chang ganglia and then from the Chang ganglia you gave off the postganglionic motor neurons and then what happened these guys we said came as a part of the cardiac plexus went to the heart to where the SA notice and it also gave fibers to the ventricular myocardium and it also gave fibers to V AV node well if we inhibit if we inhibit these fibers so if you've inhibited the cardiac accel Tory Center the action potentials that are moving down these fibers are going to pretty much decrease or be completely absent if these decrease or become completely absent are you going to be stimulating the SA node anymore with adrenergic Drive releasing norepinephrine no so that's not going to be having any stimulation AV node won't be getting any stimulation from the sympathetic nervous system and myocardium won't be getting any innervation from the sympathetic nervous system right same thing with the vasomotor Center remember the vasomotor Center brings down fibers that also is upcoming a part of the t1 l2 region and this gives off fibers that does what these fibers come out to a Chang ganglia and they go to a specific area what is that area remember they go to an actual arterial or the smooth muscle is what would that muscle here in the area call it was called the tunica media if you guys remember we have it's called the tunica media it's a smooth muscle layer in the blood vessel well hearing the arterioles we're going to have tunica media with sympathetic receptors which is remember releasing neuro epinephrine but in this situation what's the problem we inhibited this system so if this system has been inhibited here's the vasomotor Center this is inhibited it's going up at the action potentials and so there's going to be pretty much no action potential are very little action potentials that are being moved down these sympathetic nerves if you're releasing very little action potentials then you're going to release pretty much no norepinephrine if norepinephrine is not acting on these beta I'm sorry alpha 1 as metric receptors it's not going to be constricting the vessel if it doesn't constrict the best of what happens so if there's very little so let's actually not get rid of let's say that pretty much norepinephrine release significantly decreases or just completely becomes null in this point then whenever it acts on this area this receptor is going to be inhibited in this case because it's not going to have any type of stimulation by the norepinephrine what's that for except there was this again alpha 1 a generic receptor if this is the case then if this smooth muscle is not receiving norepinephrine then the muscle the actual smooth muscle is going to relax so there's going to be relaxation of smooth muscle or the tunica media in this case right if the smooth muscle relaxes what starts happening to the actual diameter of the blood vessel starts getting bigger what is that called when the blood vessel starts increasing in size the lumen gets bigger it's called vaso dilation and what does vasodilation do it increases the diameter what's half of the diameter call radius if you increase radius what's that formula called push cells equation which says that radius is equal to 8 times the viscosity times the length over PI R 4 if I increase the radius it's going to do what to the actual resistance it's going to decrease the resistance significantly because these are inversely proportional so the resistance the total peripheral resistance is going to significantly decrease so now if I decrease the total peripheral resistance what would happen anything to do with this well if you guys remember we said that blood pressure is equal to cardiac output times total peripheral resistance well I significantly decreased my total peripheral resistance what is it going to be the blood pressure it's going to decrease the blood pressure so as a result what's going to happen I'm going to decrease my BP and that was one of the problems was where I had too high of a BP I just kind of addressed it right there by doing what to the blood vessels dilating them decreasing the actual resistance so that's one way that we can fix it so again one way that we're going to fix this is we're going to inhibit the vasomotor nerve center which is going to basically decrease the sympathetic impulses that are going to the tunica media if you decrease the sympathetic impulses that are going to the tunica media then what's going to happen you're going to release less or pretty much no norepinephrine is less norepinephrine or pretty much no norepinephrine is being released you're not going to be causing the smooth muscle to contract anymore so now the smooth muscle will start relaxing as the smooth muscle starts relaxing it starts dilating increasing the diameter which increases the radius and then decreases the perf resistance which increases your blood pressure okay and if you really want to be particular technically increasing the toilet one you ever you change your total peripheral resistance you're really changing your diastolic blood pressure so really if you really want to be particular this decrease in blood pressure is really diastolic is really the one that's actually decreasing alright that's good enough now what about this darn oh wait one more thing what about this number we had these fibers these weird fibers that actually come completely out they don't actually stop at the Chang ganglia they pass through the Chang ganglia and they come to the adrenal medulla where the postganglionic fibers are and these postganglionic fibers release certain chemicals what were those chemicals here called it was called epinephrine and norepinephrine and if you remember 80% of it was epinephrine and then 20% of it was norepinephrine in this situation this process is not going to occur that much right so you because you're inhibiting a lot of these sympathetic fibers so if you inhibit the sympathetic fibers you inhibit the actual adrenal medullary fibers if this is inhibited I release pretty much no epinephrine and no norepinephrine if these are decreased this can also remember epinephrine also binds on to the alpha-1 adrenergic receptors so if epinephrine is also inhibited in this area because epinephrine which was released by the adrenal medulla also likes to act in this area but in this case there's a very very low level of him and that is because there's the inhibition of the cardiac excel at Horry Center sweet deal now let's get into this green guy here okay what is this guy here called very very important one this is the cardiac inhibitory center and again we said it's a part of the dorsal nucleus of vagus the vagus nerve cranial nerve 10 he has these fibers these gve fibers okay that are going to come out and as they come out they're going to give these connections here primarily they're going to come through a specific type of plexus like system here and they're going to give way to the essay notes they're going to get fibers to the SA node and they're going to give fibers here to the AV node so again what fibers is it going it's going to be going to the AV node and it's going to be going here to the SA node so it's also going to be giving fibers to the sinoatrial node or the SA node and the AV node of the atrioventricular node now when it goes to this area and it acts on the SA node of the AV node what is going to do also you actually even add onto this more let's say that I have the heart here I'm going to draw just a quick diagram of the heart here Kru diagram let's say here's the SA node here and here's the AV node right here if we really want to be particularly the actual right vagus innervates the SA node and the left vagus nerve is when innervate the AV node so again what Vegas would this be right Vegas you might see model that's not that important it is significantly important okay this can determine a lot of different things that this is damaged okay if there's some type of severing of this nerve okay so left Nega supplies the AV node right vagus supplies the SA node okay cool now question is how does this parasympathetic or these vagal fibers influence the AV node in the SA node you also might have noticed I need to make this very very very clear watch this see these let's say that this is also the vagus and it's going to be going to the myocardium of the heart these are pretty much null there is almost no innervation to the myocardium I need to make that very very clear here there is pretty much no innervation to myocardium the actual contractile unit there is innervation to the SA node the AV node and AV bundle in the Purkinje system but no innervation to the muscle of the heart the myocardium the contractile unit okay what I want to do is I want to zoom in on this actual cell and see how the acetylcholine is actually acting on the SA node an AV node on what it's doing let me real quickly come down here and I'm going to draw here self let's just say I zoom in on this SA node or AV node so what kind of cell is this SA node or it could be an AV noodle cell where could be any part of the actual conduction system again bundle of hiss right left bundle branches the Purkinje system whatever but these are the two main ones if this vagus nerve comes over here let's say here is the vagus nerve and it releases out these fibers it releases out a specific chemical it releases what's called acetylcholine acetylcholine will bind onto special receptors present on the SA node or AV node membrane called muscarinic type 2 receptors okay when it binds on to these muscarinic type 2 receptors it activates what's called AG inhibitory protein what happens is is G inhibitory protein is going to bind on to a dental a cyclist let's say here is a dental 8 cyclase but what it does is it inhibits adenylate cyclase so now identity cyclase can't convert ATP into cyclic A&P so cyclic AMP II levels are going to decrease if cyclic AMP e levels decrease the protein kinase a levels decrease if this decreases remember those special channels that I told you to remember that we're very important they were on the cell membrane and they were for the calcium these channels were very very sensitive to phosphates remember protein kinase they could philosophy relate these well guess what this is not longer going to happen in a calcium entry is going to be decreased another thing that happens here is G inhibitory there's actually three components of it one is what's called the alpha inhibitory that's the part that actually goes here and binds out to adenylate cyclase the other part is a beta inhibitory and a gamma inhibitory unit the beta and gamma inhibitory unit go over to a special channel in the cell membrane and this channel is called a potassium channel and what it does is it binds on to a little pocket here on this channel so here is going to come over here this beta and inhibitory subunit which we can say are combined here in this case these two are going to come over here and they're going to bind onto this potassium channel when they bind onto the patan Timm channel it opens up the potassium channel and potassium starts leaking out as potassium starts leaking out into the cell we'll start tapping to the inside of the cell it starts becoming very very negative as it starts becoming very negative what happens to the internal environment of the cell it starts hyperpolarizing so what's the overall effect here there will be hyper polarization if you hyperpolarize the cell it's going to take a longer time for it to send action potentials so if there's a longer time to send action potentials what is this going to do the heart rate that means the heart rate will decrease if the heart rate decreases what does that do to the cardiac output it decreases cardiac output if you decrease cardiac output you decrease blood pressure okay and how do I know that heart rate will increase cardiac output mean decrease heart rate will decrease cardiac output because there's another formula this formula is that saying that cardiac output is equal to the heart rate multiplied by the stroke volume so again if you decrease heart rate you'll decrease cardiac output in your decrease your blood pressure and again that's what we're trying to do here because the blood pressure is too high now you might be like oh what doesn't affect the contractility zarg no no innervation to the myocardium so it does no contractility effect let me get another term club straight here if this is acting on the heart rate if you're trying to change the heart we'll talk about this more cardiac output but whenever you're trying to affect heart rate and you're inhibiting your decrease in the heart rate that is called negative chrono trophic action okay so acetylcholine or parasympathetic nervous system has negative chrono tropic action in other words they are trying to decrease the heart rate whereas the sympathetic nervous system has positive chrono tryptic action it tries to increase the heart rate and it acts on the myocardium it tries to cause contractility so the sympathetic nervous system also acts as a positive inotropic agent okay but the parasympathetic has no effect or no innervation to the myocardium so it can't control the contractility okay so so far what are we been able to do we've decreased the heart rate in this person so they might have some Braddock kardia we decrease the amount of epinephrine and norepinephrine release from the adrenal medulla so that will decrease the vasoconstriction response we inhibited the vasomotor nerve fibers that are going to the vessels and decrease the amount of norepinephrine released so that we're getting we're decreasing the vasoconstriction instead we're relaxing the blood vessels dilating them and decrease in the total peripheral resistance that's the way that we've dealt with it so far we also inhibited the cardiac Axela Tory Center to inhibit the sympathetic drive to the heart these are beautiful things but we still have to see how the body deals with it again even a little bit more if you guys remember in low blood pressure in low blood pressure okay just so we're very very clear here whenever there was low BP because I want to make a correlation here it was actually stimulating her JG cells right the JG cells in the kidney and the GE G cells and the kidney were actually producing a chemical called renin now what happened with the renin the renin came into the bloodstream and if you remember there was another protein that was actually secreted by your liver and that protein was called angiotensinogen Tinson no Jen and this chemical gets acted on by renin if you guys remember and what it does is renin is going to cleave a specific part of angiotensinogen and convert him into what's called angiotensin one so converts them into a special chemical called angiotensin one then what do we say happens with the angiotensin one angiotensin one goes to the lungs whenever it gets to the lungs what happens there's a chemical in the lungs right there's a special type of enzyme that enzyme is called angiotensin converting enzyme what happens is angiotensin converting enzyme acts on angiotensin 1 and does what converts angiotensin 1 into angio tenzin - and if you remember this is the culprit he was causing so many different problems right by trying to increase our blood pressure well guess what we have a special system inside of our heart you know in our heart we have special atrial cells that have like a little endocrine like tissue and what happens is let's say that I take this atria here and I'm going to kind of just zoom in on it for a second let's say that I'm just kind of zooming on that atria right there right so again here's your aorta like this and then here's your ordered valve all right if I come into the atria and I start stretching the atria okay and why would the atria stretch because of a high pressure okay because of high blood pressure particularly some type of high left atrial pressure which is usually due to an increase in what's called pulmonary capillary wedge pressure if this is increasing due to high blood pressure so because of high blood pressure you're increasing your pulmonary capillary wedge pressure which is increasing left atrial pressure this is stretching the atria as you start stretching that atrium the atria has specialized in de creme like cells upon a part of it it secretes a chemical and this chemical I'm going to tempt to spell it's called atrial natriuretic peptide atrial natriuretic peptide is really really cool and whenever again there's increased blood pressure this increased stretch on the atrial walls it activates these special receptors inside of the heart that release this chemical called atrial natriuretic peptide now this is why I told you that remembering specifically what happened in a low blood pressure this is going to make a huge difference okay here we go so we have angiotensin 2 here he's one of the culprits of causing high blood pressure so usually he's one of the main causes of trying to increase our blood pressure why what were some of the things that he was doing if you guys remember one of the things that he was doing was he was coming here to the actual adrenal cortex remember there were special cells here called the zona glomerulosa cells and they were being stimulated and releasing a chemical called what aldosterone what else was happening it was also coming down here to thee what where the hypothalamus is and it was acting on special receptors that are present within the hypothalamic what were this nucleus called I'm going to denoted we already by the Supra optic nucleus it comes over here and it tries to stimulate the super optic nucleus and remember what does it do to the super object nucleus it activates action potentials that will cause the production of a hormone called anti Doretta hormone ADH we also refer to it as basal pressing so also what else is it doing if you remember it was also coming over here to these neurons that control first in stimulating thirst centers right it was stimulating certain chemicals to be released and these chemicals brought about increased thirst okay so so far what have we already noticed and that's not even it surprisingly so far we've noticed cause increased thirst it's produced ADH and it's produced aldosterone what else does it do remember has receptors on the actual that vascular smooth muscle within the tunica media there's angiotensin ii receptors right here okay there's angiotensin ii receptors so angiotensin ii can also come over here and do what he can bind on to these receptors he can stimulate these receptors and cause vasoconstriction right so you can cause vasoconstriction what else was he doing remember he was coming over in the kidney - he was coming over here to the kidney and he was acting on the proximal convoluted tubule ourselves so if you remember angiotensin 2 was also acting on the proximal convoluted tubule ourselves and stimulating this pathway to bring about more sodium reabsorption more chloride reabsorption and more water reabsorption if we have more sodium and if we have more water and if we have more chloride what does this do this increases our blood volume what do we say that as a tdv it increased the edv to increase the actual when I can write all these things but you remember it increased the edv it increase the stroke volume and increase the actual cardiac output which increase the BP so if it's doing all of that that's another thing is actually increasing the blood pressure right also if you want to remember it also act constricts what's called the efferent arteriole - so please a lot of difference also contract the mesangium the glomerular mesangial cells - not relevant in this topic but just mentioning that it does have other functions - okay so I gave you a little tidbit on angiotensin 2 but the problem that I'm trying to get to is how does this HR nature attic peptide fit into this everywhere where angiotensin 2 is acting atrial natriuretic peptide blocks so for example each one a tree attic peptide will come over here and it will block this okay it'll come over he actually shouldn't have a stimulate I should actually have an inhibit right so it comes over here and in inhibits angiotensin 2 from binding onto this receptor and angiotensin 2 doesn't bind onto this receptor then what happens there the actual smooth also starts relaxing if this fluid muscle starts relaxing it actually undergoes vasodilation if it beta values the diameter of the vessel gets bigger if the diameter gets bigger that means that the radius gets bigger if the radius gets bigger the total peripheral resistance decreases if that decreases the blood pressure decreases that's another way of fixing the blood pressure problem what else we also said that angiotensin 2 acted to stimulate aldosterone production well let's just follow this guy over here he also is going to inhibit the production of aldosterone so now the Ashura is not going to get released we'll see what he does in just a second wellö angiotensin 2 also does this Zack you said he also causes the release of ADH well guess what not anymore he inhibits the release of ADH he also comes over here to the 3rd centers and inhibits thirst if you inhibit thirst you're going to bring a lot more water No so if you're not thirsty then so if you're not going to be thirsty not gonna bring a lot of water you kind of absorb a lot of water across the GI T if you don't absorb a lot of water across the GI T then because your thirst is going to decreased if you decrease your thirst you're going to decrease your blood volume if you decrease the blood volume you're going to decrease the e DV if you decrease the e DV who decrease your stroke volume which decreases cardiac output and that then eventually decreases the blood pressure that's one way that we can fix it okay one all the way can we fix it okay well I told you it inhibits the release about doctrine and the hits to release of ADH okay we should actually bring this down here to make a little bit more conclusive here and inhibits the release of ADH there okay now if we inhibit aldosterone and we inhibit 88 release how does that affect us we'll come over here for a second where did I - Sherman Act let's do him and this red color here so let's say here's eyelid Ostrom if you guys remember what did he do remember he was a steroid hormone means him that he can pass through the actual philosophy of a bilayer he comes over here he binds onto this intracellular receptor this receptor steroid complex stimulates specific genes to produce three different types of proteins if you remember one of the proteins was for sodium channels one of the proteins was for potassium channels and then there was also going to be proteins over here in the basolateral membrane for sodium potassium pumps so what was it trying to do it was trying to bring sodium in and trying to get potassium out and then also these pumps over here we're trying to bring a lot of sodium out into that area a lot of potassium in particularly to potassium in 3 sodium out right that's tries for trying to do and what else would be trying to follow with the sodium water remember water wanted to also follow the sodium well if atrial natriuretic peptide comes over here and inhibits this action here it inhibits the action of aldosterone these channels are not going to be plugged into the membrane that means that you're not going to reabsorb sodium that means that a lot of sodium and a lot of the water are going to go where they're going to get lost in the urine and you're going to yearn a whole bunch of salty and watery urine if I go ahead and pee out a lot of salt and a lot of water what am i losing I'm losing fluid volume that means I'm having polyuria I'm having poly area I'm urinating a lot so I have an increase this means increased urine output okay how does this affect it that means I'm trying to decrease my blood volume if I decrease the blood volume I decrease the edv if I decrease the EBV I decrease the stroke volume if I decrease the stroke volume I decrease the cardiac output which decreases the blood pressure holy crap right so that's one way okay what about ADH let's do ADH in this brown color here ADH was coming over here at the collecting duct if you guys remember it was acting on v2 receptors and then when it was acting on the v2 receptors it was stimulating basically the plugging in of these channels remember these channels here they were the aquaporin two channels aq two proteins so it was plugging these guys into the membrane by working through the protein kinase a pathway and they were trying to bring what type of water Molitor bring water in if a tree and a theoretic peptide is present he is going to inhibit the ADH from being able to act on this receptor so then what happens all the water that you are trying to be able to reabsorb gets lost in the urine and again this also contributes to the poly area which is also referred to as increase urine output you lose more fluid volume which decreases your blood volume decrease your edv decreases your stroke volume decrease your cardiac output and decreases your blood pressure holy sweet goodness okay so that's the way that it's dealing with it now because of this because the actual our body trying to be able to bring our blood pressure back down what did we see a relationship to these formulas we saw the change in the heart rate so how did our body try to deal with this high blood pressure one way as you try to decrease the heart rate right through the vagal motor system by acting on SA node Navy node which decrease the cardiac output again if you decrease the cardiac output you decrease the BP another way is we try to act a release atrial natriuretic peptide if you release atrial natriuretic peptide what is it going to do it's when hibbett the release of ADH is can inhibit the release of aldosterone it's going to inhibit the third centers which is going to cause for you to lose a lot of fluid volume if there's a lot of fluid that's being lost in the urine or not bringing in water through thirst mechanisms then what's going to happen the blood volume decreases and that decrease the stroke volume if you decrease the stroke volume you decrease the cardiac output and again if you decrease the cardiac output you decrease the blood pressure the other mechanisms was that we were inhibiting in the vasomotor nerve center so it wasn't released in Norman Efrain we were inhibiting the cardiac accel Tory Center and that was also inhibiting the release of epinephrine so there's decrease up in Africa release and atrial natriuretic peptide was inhibiting angiotensin 2 if you inhibit angiotensin 2 UD you actually going to do what to the radius you increase the radius of the blood vessels because you dilate them that decrease the resistance if you decrease the resistance you decrease the blood pressure and this is the way that our body tries to compensate for high blood pressure our initiatives I hope all of this made sense I really really do I hope you guys did enjoy it if you guys did please hit the like button comment down the comment section and please subscribe alright news nerds as always until next time

Channel: Ninja Nerd

Views: 149,063

Keywords: hypertension, Blood pressure regulation, blood pressure physiology

Id: CnWFcOJBqRk

Length: 36min 4sec (2164 seconds)

Published: Tue Aug 01 2017