Musculoskeletal System | Smooth Muscle

I'm engineers in this video we're going to talk about smooth muscle specifically the different types of smooth muscle and how its contracting now it's relaxing let's dive right in so first off what we're going to look at here is we're looking at a huge I'm just taking blowing up one big smooth muscle cell I'm blowing that sucker up so we can see inside of it and all these mechanisms are occurring inside we're going to get to this last cos there's going to be a lot of stuff so hang in there okay now what I want to do first is I want to talk about a couple characteristics of smooth muscle the types of smooth muscle and how it's actually controlled you know some of it's actually on its own intrinsic activity some was controlled by the autonomic nervous system some are controlled by hormones and chemical factors let's talk about all that first thing I want to do is I want to take a look at one smooth muscle cell so first thing about smooth muscle that I want you guys to remember I'm going to write it down is that change muscle is not striated you have to remember that smooth muscle is not striated so first thing right away not striated first off the question at hand is what is Sri a shoe you guys watch the skeletal muscle videos you've probably heard of a term called the sarcomere remember the sarcomere was consisting of the Z disks the thick filament which is consisting of the myosin the thin filaments which had the act and the tropomyosin the troponin all that different structure that was setting up a nice nice striped structure is called the sarcomere right and that was what's making that striped appearance in smooth muscle they do not have a sarcomere okay that's one thing instead they're myofilaments or they're protein filaments are arranged in a different type of way let's take a look at that real quick and go over some of the actual microscopic anatomy of this actual smooth muscle cell because all of the others who muscle cells are going to be the same so first things first smooth muscle is generally uni nucleated because that's the first thing so let's write that here first it's generally uni nucleated meaning that it only has one nucleus where a skeletal muscle if you guys remember its multinucleated cardiac is usually using nucleated also next thing this bread structure here is representing the plasma membrane or the sarcolemma the next thing is this green structure you see all these green dots all over the actual smooth muscle cell these green dots are special special structures called dense bodies and dense bodies are made of a protein primarily called alpha actinin alpha actinin is the primary protein that's making up these dense bodies so your densities are scattered all throughout the actual smooth muscle cell what's important is that these dense bodies are anchored to the plasma membrane by these pink proteins these pink proteins are basically angry-looking this actor right here is anchoring the actual dense bodies to the actual smooth muscle cell membrane and there's many proteins that are making up that structure but basically what it's doing is there's these like attachment plaques these integrin proteins that are actually on the inner cytosolic side of the smooth muscle cell and these attachment plaques these attachment plaques are basically what these dense bodies are connecting to okay the other thing that's really really important is these orange proteins you see these orange proteins here it's connecting that dense body to that to that dense body connecting that dense body that that did that dense body and that's connecting that dense body that dense body is basically what it's doing is it's connecting the dense bodies to one another what is that orange protein called that orange protein is actually your intermediate filaments so what is this orange protein you're called is your intermediate filaments and this composed composed of two primary proteins one is actually called vine Menten and the other one is called desmond okay so so far again we have smooth muscle cell membrane which is the sarcolemma plasma membrane uni nucleated dense bodies consisting of alpha actinin the dense bodies are anchored to these attachment plaques which are just basically integrants on the smooth muscle cell membrane via these myofilaments the dense bodies are anchored to one another through these intermediate filaments made of I meant and and Desmond and here's the good stuff if you look here these dense bodies coming off of them they have these little baby blue filaments coming off these baby blue filaments are actually called your thin filaments it's called your thin filament and it's made up of two proteins one that's going to be actin primarily that of s actin and the other one is actually going to be Tropo myosin okay so on the thin filaments the thin filaments are going to be consisting on a protein called actin and tropomyosin then you're going to see in between interdigitating so if imagine here if I have my fingers here's my fingers are the actual actin in between these actual vegetations is going to be your stick filament this red line that red line structure is actually called the thick filament so again what is this red structure right here interdigitating between these thin filaments that is your thick filament and the sixth element is important because it's actually composed of the primary molecule called myosin technically it's actually type 2 okay and we've talked about myosin plenty in the actual skeletal muscle so again why is this important well whenever it different from skeletal muscle because when skeletal muscle contracts it basically causes the muscle to shorten right by moving the thin filaments closer one of those sliding those moments over same thing happens but instead the dense bodies are acting like your z disks and whenever this dense body whenever your muscle contracts it pulls this dense body right here to this dense body right here and causes these to shorten but when that one does it same thing happens right here this shortens this shortens this shorts and not only that but these actual intermediate filaments made of I mention and Desmond are also pulling the actual dense bodies closer together so afterwards your smooth muscle will actually kind of twist and squeeze itself together and kind of make like an actual cork shoe type of like shape right so imagine here is that smooth muscle and then we decide like squeeze it and basically like imagine it like this and now imagine just I'm going to draw all of these just random but imagine here is all of these actual dense bodies and thin filaments and thick it's basically squeezing that smooth muscle sound like a corkscrew like action okay all right so that's the microscopic anatomy of the smooth muscle cell next thing we need to talk about so you know that smooth muscle cells not striated and we know why because it doesn't have a sarcomere it has all of this actual protein structure next thing we know it needs we need to know the types of smooth muscle so there's two types of smooth muscle one is actually called unitary smooth muscle they also call it single unit smooth muscle smooth muscle smooth muscle this is actually also called visceral muscle so this is also called visceral smooth muscle because this is primarily where you're going to find this type of muscle the other one is going to be multi-unit smooth muscle multi-unit smooth muscle all right sweet deal now what's the difference between these two well one thing that you probably already going to get out of this is that unitary is also called visceral smooth muscle so where would you find it you find us within the GI tract you find it within the urogenital tract just the first thing so let's mark that out where would the location where would you find this type of smooth muscle again you find it within the entire length of the gastrointestinal tract you'd also find it within the actual uro genital tract okay so pretty cool stuff there now the multi-unit smooth muscle where would you find that one this one is primarily located in a couple different places and we'll talk about why they're found in different places because obviously due to their function this one is primarily found within like the iris so specifically you know how you have the IRS you have the pupil a sphincter and you have the dilated pupil a right so the actual iris has the dilator and the constrictor pupil and so the constrictor pupil a these muscles are actually a specific type of multi-unit smooth muscle another type is actually going to be the bronchial smooth muscle so the bronchial smooth muscle is also multi-units the tunica media which is inside of our actual large vessels so inside of our large arteries large arteries very very thick tunica media layer within a large arteries and you can also find this within another part of the eye which is called the ciliary muscles which control the actual lens so they control the lens the accomodation action and you can even find these suckers in the erect or peel eye muscle which basically gives you the goosebumps this is the goosebump muscle alright alright so we deal so we know where we find this one now why will we find in this one the next thing we need to understand is that these unitary smooth muscles are actually interconnected with one another they're interconnected with one another especially through these specialized structures called gap junctions and gap junctions just basically connects and subunits and let's say that another thing it's actually innervated by the autonomic nervous system most of our actual smooth muscle is innervated by the autonomic nervous system it can be affected by hormones or other chemical factors like we said but generally autonomic nervous system via the parasympathetic nervous system or the sympathetic nervous system has effects on this actual smooth muscle and it has you see these little balls right there there's little blue balls that I drew right there let's expand in on one of these this is actually consisting of multiple different types of neurotransmitters these blue bulbs which are basically these synaptic vesicles are consisting of various neurotransmitters and they call this bulb of varying our transmitters they call it a varicosity okay a varicosity and varicosities consists of many neurotransmitters for example you can release norepinephrine it could release acetylcholine it could release neuro as our nitric oxide you could release adenosine it can really substance P many different chemicals we're not going to go over all the chemicals but it can really so many different chemicals from these varicosities and they can act on the smooth muscle ok so again it can be integrated by the autonomic nervous system both the parasympathetic and the sympathetic as well as hormones and other chemical factors here's the crucial thing let's say that these neurotransmitters are released from these varicosities so let's say that these varicosities are releasing chemicals and it's stimulating these smooth muscle cells right here what's cool is if it only stimulate these smooth muscle cells you're like oh wait we'll only only those ones are going to contract now they have these electrically coupled gap junctions that allow for ions to flow from this cell to this cell to cell such as one cell to cell three cell I can have these cations flowing from this cell into this cell stimulating that cell and then flow in from the second cell to the third cell stimulating this one then hook it can flow over into the fourth cell and stimulate this bad boy pull over here to the 5th cell and stimulate this bad boy and it can also flow into the sixth cell but this is already getting stimulated but you get the point all of these are electrically coupled together so they're electrically coupled together so because of that they can generate a rhythmic and syncytial contraction so they can generate a rhythmic simultaneous contraction it's pretty sweet right yeah another thing is because this is actually going to be in the GI tract and here a genital tract this isn't really for very fine tuning activity which is like within the iris and the bronchus move mouse on all these other structures those are like well you know there's the difference being gross control and fine control so like for example and I'm applying this to more of like a larger concept and we're going to apply to the smooth muscle grouse control is like me moving a whole arm and gets me moving a whole arm are picking something up utilizing a lot of that action right there if I decide to watch this I take and I pick up this pin I picked up the marker I used very very fine control so find controls like very very small movements whereas gross controls very very large and powerful movements this is meant for very very gross control heavy powerful movements so let's write that here so this is for gross control which is just heavy powerful movements now with this one look at these suckers they're all separated from one other there's no gap junctions connecting these guys so they each one of them have their own stimulatory neuron so because each one of them have their own stimulatory or it doesn't always have to be stimulatory remember that it could obviously be inhibitory but we're talking about it with a sense of stimulation again all of these neurons have their own nerve ending this has its own nerve ending this has its Nova nerve ending this has its own nerve ending this has its own nerve ending they're not electrically coupled together so they don't really work in a sense ischial like action they're not really going to develop a rhythmic contraction they are structurally independent of one another so let's write that there they are structurally independent alright so this one you would actually see because they have so much nerve endings they're actually going to be very excitable so these are more for the concept of fine control very very fine controlled activity ok all right so sweet vo so we now we understand that so that's the difference between unitary smooth muscle multi-unit smooth muscle one more thing I said is that our smooth muscle is generally controlled by the autonomic nervous system right whereas if you guys remember from the skeletal muscle which is controlled by the somatic nervous system so let's compare the two that quick autonomic nervous system is composed of the parasympathetic nervous system and it's composed of the sympathetic nervous system of putting SNS for sympathetic nervous system parasympathetic nervous system for PSNS these are going to directly control the actual smooth muscle they control smooth muscle and cardiac muscles so smooth and cardiac but the key thing is is that this is all involuntary we do not have any conscious control over this some people might have the ability to do it through biofeedback techniques but we're talking about this in general the somatic nervous system is what's controlling the actual skeletal muscle and this is actually going to be voluntary so I just want you guys to understand the difference between the smooth muscle as compared to the some of the actual skeletal muscle all right now we've done that ok now what I want to do is I'm going to look at a smooth muscle cell and I want to see how we can actually stimulate the smooth so through various different types of stimulation as well as intrinsic stimulation that's going to be pretty cool to see and then we're going to see all the mechanisms that are occurring intracellularly and then we're going to see the contraction process and then we're going to see the relaxation process okay so let's start there first the first thing I want to do that I want to make a graph let me make a graph real quick here small graph would have to be a really big one I'm going to put this one right here okay and what this graph here is going to represent is I'm going to have a resting membrane potential denote that is RMP and that's going to be approximately around negative 55 millivolts I'm sorry not negative 55 that's a wacko move there should be negative 80 millivolts about okay and then let's say that they have a threshold potential and that threshold potential which I'm gonna demo is TP let's say that's around negative 55 millivolts okay and then they have a peak potential but we'll talk about that what's really cool about this is that certain smooth muscle cells primarily that of the unitary or the visceral smooth muscle which is in like your stomach and your small intestine a large intestine they have this really cool like rhythmic pacemaker like activity they're specific cells and these cells are called the interstitial cells of casual or kajol however that conveys name either way these are your pacemaker cells okay so these are your pacemaker cells what does that mean to be a pacemaker means it can intrinsically depolarize dependent of any extrinsic innervation like a nervous system how do they do that this is so cool let's do this one in a pink here what can happen is look at this it has here's a resting membrane potential it can actually produce these things called slow waves and these slow waves can get pretty darn close to threshold potential and sometimes actually break threshold potential what are these little slow waves due to because generally a smooth muscle cell has a resting membrane potential that's pretty very stable and then it based upon a simulation it'll rise this can do it on its own these little pink up-and-down waves are due to two things inside this smooth muscle cell in certain smooth muscle cells we're going to talk about pacemaker cells they have these specialized stretched like calcium channels look like here at the top here we have the stretch sensitive calcium channels I'm sorry I'm not sure shouldn't they stretch incitive I should just say leaky let's just a leaky leaky calcium channels leaky calcium channel so in other words they're kind of like always open what are these leaky calcium channels doing they're constantly staying a little bit open enough for calcium to actually rush into the cell not excessive but very very slowly a very very slow flow of calcium into the cell if calcium is constantly flowing into the cell what are we bringing into the cell we're bringing positive ions into the cell as we start bringing positive ions into the cell what starts happening to the membrane potential it starts becoming more positive when did you see that from let's come back down look it was right from this part so this rising part of the slow wave is actually due to calcium ions and again one of the way that we call these these things right here where you go up and down up and down very very slowly is called slow waves it's basically the basic electrical rhythm and again whatever these slow waves do - they're due to these calcium channels that are constantly leaking allowing for little bit of calcium to come in well why does it go back down well because potassium channels open so then what happens is potassium channels will open whenever it goes up and it doesn't hit the threshold so let's say that it goes up doesn't hit the threshold so it goes up doesn't hit that dotted line and it goes back down what would that be due to it would be because on the membrane you're going to have these potassium channels these leaky potassium channels and these potassium channels are going to keep flowing out of a cell until they reach their equilibrium or Nernst potential positive ions are going out of the cell then the inside of the cell become more negative and as you tries to become more negative it brings the resting membrane I'm sorry the the actual membrane potential back down to rest okay if do we don't reach threshold but let's say some chance that actual slow wave breaks threshold just enough let's show that it breaks threshold just enough those calcium channels are open up long enough to break the threshold point if it breaks the threshold point look what happens here let's do this in this blue color you get these things here where do you just break the threshold potential boom look at this you produce these things called spike potentials so you produce these things called spike potentials which are basically action potentials these are basically action potentials and what do they do - okay so let's say that you hit the threshold potential if you hit the threshold potential these are here called voltage-gated calcium channels and these voltage-gated calcium channels are usually located in these little divots you know our actual smooth muscle cells are different from the skeletal muscle smooth skeleton also has the t tubules instead of that we have these things called Calvillo oleh they're just these tiny little kind of like little divots and inside of those divots we're going to have those voltage-gated calcium channels so all I'm doing right now is I'm zooming in on one of these voltage-gated calcium channels these little channels these blue channels that we show within these little divots with these little divots here called again they're called Calvillo ley caviola the little divots that basically similar to the tee to businesses and skeletal muscle we said right now these voltage-gated calcium channels are going to open right and they're going to open whenever that actual slope these little leaky calcium channels causes it to hit let's say that they hit threshold potential if they hit threshold potential that will stimulate these voltage-gated calcium channels the voltage-gated calcium channels will open if the voltage-gated calcium channels then calcium will start flooding in extremely fast so this would be a fast flow of calcium and what will happen to the inside of the membrane they'll become extremely positively charged right and when it becomes extremely positively charged what's that going to do it's going to cause the actual a lot of different things to happen specifically if the calcium starts flowing in the membrane potential flow really really high let's say it reaches a point here of about positive 30 millivolts and then it will go back down what will cause this by potential to go back down it'll be due to these potassium ions leaking out of the cell but specially more specifically these voltage-gated potassium channels are going to be these voltage-gated which kind of like these calcium sensitive potassium channels and potassium will start leaking out making size making the inside of the membrane more negative to relax okay but if occur very rapidly and again if that was that one and it still has a threshold another spike potential will occur if it's still a threshold it'll hit another spike potential so in other words watch this let's say by some situation we have some other stimulation factors and that's we're going to talk about here let's say by some situation we have those leaky calcium channels but then we blow past the threshold potential like what what could actually cause us to go even more than the threshold potential you know there's certain types of chemical factors so in certain situations but especially in smooth muscle protons have the ability to act on smooth muscle oxygen has the ability to act on smooth muscle co2 has the ability to act on smooth muscle and depending upon their levels they could either stimulate or inhibit the smooth muscle to contract so this could stimulate the smooth muscle contraction or they can inhibit the smooth muscle contraction what else in our nervous system I said that our nervous system let's say that for some situation here you're releasing acetylcholine acetylcholine is for the most part and our actual smooth muscle generally depending upon what organ in this case we can say that this is a smooth muscle cell of the stomach if it is a feel choline would love to stimulate this one by acting on what's called muscarinic like three receptors but at the same time we can have other parts of the nervous system come over here and if that was that case let's say that it released Noro epinephrine norepinephrine would want to inhibit this actual smooth muscle via certain types of adrenergic receptors okay now if this were to happen that could also affect you know what else can also affect it too besides these chemical factors besides these neurotransmitters so what would these be due to this would be doing neurotransmitters there's other things that can affect it also hormones so today I have another receptor here another receptor hormones can also directly affect this like what type of hormones they can either stimulate or they can inhibit it depends on what hormone it is could be hormones like cholecystokinin it could be hormones such as histamines it could be hormones like gastrin there could be many many different hormones but hormones have the ability to either stimulate or inhibit this actual smooth muscle in other words cause it to contract or to relax how would it cause it to relax it would basically inhibit a threshold potential it cause negative ions to flow into the cell or positive ions to come out of the cell how would it stimulate it would cause cations to flow into the cell so if you wanted to stimulate this you'd want positive ions to flow into the cell if you'd want to inhibit this you'd want specifically the positive ions to leave the cell because this would cause the inside of the cell become very negative if positive ions are coming in this would cause the inside of the cell to become very positive and it will approach sexual potential or even break the threshold potential same thing with all these other guys but now let's talk about the most important thing which is the actual of nervous system so let's say the neurotransmitters right from what our nervous system let's say that you want to contract a smooth muscle so say that we have this acetylcholine acting here acetylcholine will act as muscarinic type 3 receptor when it does it'll activate what's called AG cue protein when it activates this GQ it will activate another protein which is called I'm sorry activate an enzyme called phospholipase c and phospholipase c is really special because what he'll do is he'll degrade to different chemicals one chemical he'll degrade is actually going to be the degrade what's called pip2 which stands for fossil in a SCYTL diphosphate what he'll do is he'll break this actual chemical up into two components one of the components is actually going to be in a Seidel triphosphate ip3 the other one is going to be called da g which is diacylglycerol this will go on to activate what's called protein kinase C which can go and phosphorylate many different types of enzymes and proteins but this is the important bugger right here ip3 has specialized channels on this blue structure here what is this blue structure here called this is called the Sarco plasmic reticulum we already know that this is a calcium storage Factory and inside of this sarcoplasmic reticulum we know that we're going to have a lot of calcium ions but what else do we say was special about the sarcoplasmic reticulum besides having a lot of calcium ions remember we had these specialized proteins that were holding onto the calcium ions remember these suckers right here that we're holding onto them like the cal sequestering and the calreticulin so you're also going to have these proteins which again is the cal sequestering let's draw a green one here and this green one here could be the calreticulin and these proteins are basically concentrating the calcium inside of the sarcoplasmic reticulum and again one of these proteins let's say that this is called Cal reticulum and let's say that this red one right here is actually going to be called Cal sequestering Cal sequestering what happens is when this ip3 comes over here binds on to this ip3 receptor and it stimulates this IP 3 receptor and causes the calcium ions to flood out and this increases the calcium ions in the cell what else increases the calcium ions in the cell well we already said it could be due to these leaky calcium channels right the calcium will flow in a little bit it'll activate thresh will bring it to threshold potential and cause this voltage-gated calcium channels to open and cause calcium to come in so this will also increase the actual cellular calcium so how many ways if we increased calcium levels one way is going to be through these voltage-gated calcium channels on the actual membrane what could open these these leaky calcium channels could maybe hit threshold potential or we could have other things influencing and bringing this actual slow waves above threshold potential like what like hormones like certain chemicals like neurotransmitters or a big big one this is huge stretch stretch also stimulate these leaky calcium channels if I stretch the smooth muscle it stretches out these calcium channels if I stretch out these calcium channels a little bit more it's going to make the channel a little bit bigger and guess what's going to flow in more you're going to have a little bit more calcium flowing in if a little bit more calcium flows in what's going to happen to the membrane potential it can make it more positive if it makes it more positive one that stimulate threshold potential yes and that'll cause these voltage-gated calcium channels to open in calcium will rush in so one way that we got the calcium in was through these voltage-gated calcium channels a second way as we did it through a second messenger system so the second way was through the second messenger system which could be due to hormones also remember hormones can also trigger this process to to increase the calcium levels by certain mechanisms okay primarily through this ip3 mechanism there's another we can get calcium you know whenever our calcium levels let's say that we're pulling a lot of this calcium out of the sarcoplasmic reticulum as the calcium levels inside of the actual sarcoplasmic reticulum starts depleting then what happens is our sarcoplasmic reticulum makes a very interesting protein look at this protein it expresses this protein and this protein comes up to the membrane and it's like basically kind of like coming up to the membrane and saying to the membrane hey I need some guys over here he calls a guy named array he's like oh hey come here buddy and what happens is this array protein these tetra Murs what do these thing called they're called Oh Bray hatch rumors they're basically these what's called store operated calm calcium channels stocks and what happens is these over a molecules start binding to this black protein and I'll tell you what this black protein is in just a second and what happens is as they start binding this black protein is actually called stim it's a stim protein okay it's called stim and this one right here these actual proteins are called over a proteins okay what happens is whenever the calcium levels are depleted it stimulates stem and stem stimulates the over a tetra MERS to aggregate and guess what happens it opens up the extracellular fluid into the intracellular fluid and calcium starts rushing in when calcium rushes in he's inside the cell now how do we get them in back into the SR to control the actual levels there's specialized channels right here these specialized channels will actually bring the sodium ions out and bring the calcium ions in and there's also proton channels too so you know there's other ones here too which can actually bring protons out and bring the calcium in but this step requires ATP remember that right alright so either way we got the calcium inside of the cell and it can fit into the actual pacemaker activity or it could be the hormones if you do two chemical factors could be due to neurotransmitters computer stretching of leaking calcium channels but either way we can get it in through the voltage-gated calcium channels we can get it in through the store operated calcium channels we have the over a tetra MERS in the stem or we can get it in through the ip3 receptors via hormones or neurons okay hormones are neurotransmitters so this was the third way okay now once this calcium is in that was the overall thing that the calcium levels are rising let's say that over here so the overall effect was the calcium levels were rising inside in itself that's awesome because you want to know why people be like oh doesn't it just go and buy on troponin there is no troponin I'm sorry there is no troponin yes there's a component inside the actual smooth muscle instead there's another molecule this other molecule is called calmodulin so there's another molecule called calmodulin what happens is these calcium molecules are going to come over and they're going to bind on to and when they bind onto the calmodulin you form this thing called a calcium calmodulin complex I'm going to call it take calcium cam complex why is this important a couple reasons on the actual plus do this in an orange on this actual thin filament remember we said that there was a protein here and this protein was called tropomyosin that orange protein that orange protein there is called Tropo myosin okay well that's cool but guess what else is there there's another protein and this protein is sitting on the actual tropomyosin and the actual actin what is this protein called this protein is called Cal ponen there's another protein and this protein is actually going to be over here by the myosin and this protein is actually going to be having its foot right here on the myosin as well as a foot near the actin and this guy is called Cao Desmond generally what these proteins are doing is if you guys remember from the actual skeletal muscle videos we have the myosin right here right and on the myosin head it has an enzyme here and that was called a ATPase and it was responsible for cutting ATP into ADP and inorganic phosphate that's what it was responsible for well generally what kalpona and what Cal Desmond is doing is Cal ponen is actually inhibiting this ATPase activity Cal Desmond is inhibiting this ATP's activity they're also hindering the interaction between myosin and actin well guess what calcium calmodulin complex does the calcium calmodulin complex comes over here and inhibits the kalpona and inhibits the cal desmond when you inhibit these guys they no longer will be able to inhibit the myosin ATPase activity and they're no longer be able to a hinder the actual myosin actin action and so what will happen the tropomyosin will then move out of the way so it's sure that the tropomyosin is moved out of the way and then Cal ponen is out of the way and Cal Desmond is out of the way another thing happens unfortunately right it's always something else So Cal Ozzy the calcium calmodulin complex will do another thing to come over here and you'll activate this enzyme this enzyme is called myosin light-chain kinase this myosin light-chain kinase is really special so what will happen is com module in calcium complex will come over here and stimulate this myosin light-chain kinase what the myosin light-chain kinase will do is it'll add a phosphate on to the actual myosin heads I'm sorry that's not the head the neck guys remember on this actual myosin structure here if I redraw it again let's say I redraw this again here you're actually going to have the head here you'll have the neck and here you'll have the tail right what happens is we're going to add a phosphate onto the neck specifically on what's called the regulatory light chain so the regulatory light chain so if we add these phosphates onto the regulatory light chain on the neck of the actual myosin what it's going to do is this will stimulate that myosin ATPase activity if the myosin ATPase activity is activated it'll break down ATP into ADP and n2 and inorganic phosphate so again what happens the myosin light-chain kinase comes over and phosphorylates the regulatory light chain on the neck of the myosin which activates the myosin ATPase activity to cut the ATP into ADP and inorganic phosphate now let's show that so that's happened now so phosphorylate this bad boy this bad boy this bad boy this bad boy sweet deal Nataly phosphorylated this activates that myosin ATPase activity now generally what happens is the myosin is normally bound to ATP which helps it to be able to deep Hach the myosin so let's assume that it's detached right now and then on top of that we have this floss feed bound here to the actual regulatory light chain once this happens it activates what it activates the ATPase enzyme when it activates the ATPase enzyme what does it do it Cleaves the ATP into ADP and inorganic phosphate so what is this first step here the first step is ATP we can actually say this is the second step technically ATP hydrolysis because the first step was this actual phosphorylation of regulatory light chain on the myosin then we hydrolyze the ATP into ADP and inorganic phosphate so now look here I'll have ADP and inorganic phosphate same thing ADP inorganic phosphate ADP organic philosophy ADP and inorganic phosphate and it's still what is it bound to it's bound to a phosphate here on the neck on the neck on the neck then remember what happens when you have ATP remember here's my hand is the act in my head is the myosin generally I'm attached to the actin whenever ATP binds the myosin detaches whenever I hydrolyze the ATP into ADP and inorganic phosphate it goes into the position and then reattaches to the next actin so pretend I bring my hand here and this is the necked actin then it's attached what will it do it'll release the ADP which will generate the powerstroke right so what's this next thing to happen the third thing to happen is we have to release the ADP because right now it's in the cocked position it's in the cocked position we released the ATP and this generates the powerstroke right and that was the thing I told you where if I was the my hand is the act of my head is the myosin I'm attached here ATP binds I detach hydrolyze ATP I go in the cocked position reattach released ADP I then create the powerstroke then what do i do bind ATP detach hydrolyze it go into the cocked position reattach the next released ATP power stroke and it's just going to keep happening and happening happening until we actually cause those minor filaments to slide over one another then what happens is what is it left with it's left with an inorganic phosphate but it's also still bound to this phosphate on that regulatory light chain then what are we going to do we're going to get rid of the next thing which is going to get rid of the we're going to get rid of that actual loop now let me rephrase this here we actually don't release ADP we released a phosphate that I'm sorry we released a phosphate so we should still have ADP bound afterwards so what should we actually have bound here we should have the inorganic phosphates bound we should have the ADP still bound okay sorry about that so again actin is right here myosin is the head if I'm attached I want to buy an ATP I detach if I want to it i hydrolyze it now I have ADP and inorganic phosphate and then I'm going to reattach then I release the phosphate powerstroke then what I do I get rid of the ATP ADP and rebind at ATP I detach hydrolyze it cocked position reattachment it keeps happening so now I release the inorganic phosphate I have the ADP left over I'm going to get rid of the ADP and bring in a new ATP okay so now I'm going to release the ADP and bring in a new ATP if I do that now look what happens I'm going to have the ATP right here if I have the ATP right here the inorganic phosphate is still stuck there so it'll just keep happening it'll just keep going and doing this process what if I want to stop what if I want to relax the smooth muscle guess who comes with the rescue there's another enzyme which is called myosin light-chain phosphatase and this myosin light-chain phosphatase what he's going to do is he's going to come over here and he's going to remove those phosphates he's going to get those phosphates off if he gets those phosphates off then the actual myosin ATPase activity will be inhibited so now the myosin ATPase it could be will be inhibited because you're no longer going to have these phosphates there so this ATP is that could be will be inhibited then guess what else is going to happen the calcium that's bound to the calmodulin is like dude I got to go back to sarcoplasmic reticulum is calling me home buddy so guess what he does the cow seems like Frick this crap amount and the calcium leaves and goes back to the sarcoplasmic reticulum via these calcium sodium exchanges so they called in the Circa or through these actual calcium atpase --is so either way it's getting back into the sarcoplasmic reticulum if that happens what happens to the cam calcium complex it decreases what happens to the kalpona and inhibition that goes away what happens to the myosin light-chain kinase activity that goes away so this is going to be inhibited this will now be stimulated to go back into action so now the cow ponen will be stimulated to go back into action the caldez main will no longer be inhibited so he'll be stimulated to go back into action and then it will inhibit the myosin ATPase activity if you inhibit the myosin ATPase activity then it's no longer going to continue to break down the actual ATP then what happens the tropomyosin goes back to his normal position blocking the myosin from binding to the actin but that's not it some of this calcium can also get out of the cell too - no there's actually specialized channels on them cell membrane - and these channels are actually bringing the calcium out here and this could be bringing a proton in you also could have other channels which are bringing the calcium out of the cell and bringing some of the sodium ions into the cell and that can also happen but we're basically trying to get the calcium out of cell or back into the sarcoplasmic reticulum as it does that another thing happens remember those voltage sensitive potassium channels those voltage sensitive potassium channels also open and potassium starts leaking out of the cell as the potassium starts leaking out of the cell the positive ions start leaving the cell right as the positive ions start leaving the cell what happens to the inside of the cell becomes negative as it becomes really really negative then what happens the cell starts relaxing and then what would happen what would it show here on this so if we were to kind of correlate this now this last part here in this actual graph we would say this I say whatever reason we win over threshold potential we have this spike part and then what happens we have the relaxation period but then let's say that we're still here at the actual above the actual threshold what will happen there'll be another spike potential but then the cell has to relax so what will happen potassium ions will leave and calcium ions will go back into the smooth endoplasmic reticulum that's a it's still a threshold what will happen it will have another spike through the calcium entry from whatever the three ways and then what happens the actual repolarization phase due to the potassium leaving or calcium going back into the sarcoplasmic reticulum occurs all right engineers we covered a lot of information in this video about smooth muscle the types of smooth muscle how it's not straight and we went over its microscopic anatomy we went over its neural control hormonal control the chemical factors we went over the entire contraction and relaxation mechanism I really hope this made sense I hope you guys did enjoy if you did please hit the like button comment down the comment section and as always please subscribe I ninja nerds until next time

Channel: Ninja Nerd

Views: 172,397

Keywords: myology, smooth muscle

Id: 2EeUy7xopdo

Length: 45min 43sec (2743 seconds)

Published: Tue Jul 18 2017