 The factors which effect to glomerular filtration include the driving forces and the filtration coefficient. The driving force mainly includes the glomerular hydrostatic pressure which is a force promoting filtration and then there are forces opposing filtration that is the glomerular oncotic pressure and tubular hydrostatic pressure. And the second component that is filtration coefficient includes the characteristics of the capillaries that is how much permeability is and how much is its surface area. So now these are the forces what we said which affect the glomerular filtration rate. So any factor which affects these forces can affect GFR but there is a need to maintain glomerular filtration rate in a constant range for effective excretion of the waste products. So if there is any factor which tends to change this GFR, body tries to bring the GFR back into the normal range. Okay so let's see how this is happening. See anything which retains blood in these glomerular capillaries will increase the glomerular hydrostatic pressure and hence will increase the GFR. So the mechanisms which tend to change GFR or maintain GFR use this concept where they either increase the blood in capillaries or decrease the retained blood in these capillaries. So first thing is suppose if there is increase in renal plasma flow there will be increase in GFR. Now remember that flow is equal to pressure upon resistance. So whenever the blood pressure increases or the driving force what we say increases the flow will increase. Isn't it? So let's take an example say blood pressure mean blood pressure of body increases. So obviously renal blood flow will also increase. So what will happen? This will tend to cause increase in GFR. So it should be brought back to normal, isn't it? So that is done by changing this resistance. So whenever there is increase in pressure the mechanisms cause change in this resistance. So what resistance are we talking about? Here we are concerned about renal blood flow. So obviously we are talking about the resistance of the renal vessels which in this case are afferent arterioles and efferent arterioles. See the glomerular capillaries are having arterioles both proceeding it which is called afferent arterioles and also following it which we call efferent arterioles. And arterioles have a characteristic that they can contract because their balls are muscular. So when renal blood flow increases there is constriction of these afferent arterioles which in turn cause decrease in renal blood flow because it will offer more resistance to blood flow, isn't it? That will decrease GFR. On the other hand let's see another factor. Say suppose there is something which can cause efferent arterioles constriction. Actually it's caused by angiotensin. Okay? It acts more on the efferent arterioles causing its constriction. So if there is efferent arterioles constriction see the resistance of the vessels is increasing. So renal blood flow will decrease. However because it is affecting the outflow from the glomerular capillaries more blood will be retained in the glomerular capillaries. This will cause increase in GFR, isn't it? So fundamentally what I am telling is that this renal blood flow and GFR are affected independently by change in these arterioles resistance. So let's try to understand this by use of these graphs which are given in books. So in this graph you see x-axis shows the afferent arterioles resistance and y-axis shows glomerular filtration rate and also renal blood flow. So let's focus on renal blood flow first. See as afferent arterioles resistance is increasing what is happening renal blood flow is decreasing. Right? And now you see what is happening to GFR. Yes GFR is also decreasing. So whenever afferent arterioles resistance increases renal blood flow decreases. This leads to decrease in glomerular capillary hydrostatic pressure and hence decrease in GFR. Now let's see the other graph. This graph shows the effect of efferent arterioles resistance on the renal blood flow and GFR. See as efferent arterioles resistance is increasing that it is constricting more and more renal blood flow is decreasing because ultimately the total vascular resistance of the renal vessels is increasing. Right? So blood flow will decrease. But you see what is happening in GFR? Initially there is a rise in GFR isn't it? This is happening because despite the decrease in incoming due to decrease in the renal blood flow you see there is also a decrease in the outgoing. So the blood is retained in the capillaries itself causing increase in the glomerular hydrostatic pressure. That's why this GFR is increasing initially with increase in the efferent arterioles resistance. However if efferent arterioles resistance increases too much you see the incoming is decreased so much that even the GFR decreases. So why is it important to understand all this? Fundamentally body regulates glomerular filtration rate basically by changing the afferent and efferent arterioles resistance. So again let's see the example of increase in blood pressure as already told that increase in blood pressure will increase renal plasma flow which will tend to change GFR. But you see in this graph it shows that within a range of change in blood pressure GFR is held constant. This range is approximately from 60 millimetre mercury to 140 millimetre mercury of mean arterial blood pressure. So this is known as auto regulation of GFR. So how is this auto regulation of GFR done? Basically there are mechanisms which operate before filtration and the mechanisms which operate after filtration also. So the mechanism which operate before filtration is known as myogenic mechanism and that operating after filtration is tubular glomerular feedback. Let's look at them one by one. In myogenic mechanism what happens that whenever mean arterial blood pressure increases there will be increased renal blood flow in the arterioles. Now these arterioles have something called stretch sensitive calcium channels. So whenever renal blood flow increases there is opening of these stretch sensitive calcium channels causing their opening and causing entry of calcium ions. Now these calcium ions cause the constriction of the particular smooth muscle. So you see it's like a local reflex mechanism operating here. Increase in renal blood flow itself is causing decrease in the diameter of the apparent arterial and hence increasing the resistance causing decrease in the renal blood flow. So that is the myogenic mechanism. Now second mechanism is the tubular glomerular feedback. Tubular glomerular feedback basically acts after filtration and it links the changes in sodium and chloride concentration which happen in the tribules whenever the GFR changes. See if GFR increases more sodium and chloride will also be filtered and if they are filtered more despite their increased reabsorption also more will go further into the tribules. Okay so how this is done? Basically for understanding this you should understand the structure of a juxtablonradar apparatus. It is very simple. See this is the Bowman's capsule. This is the capillary showing the afferent arterial and efferent arterial. Now these afferent arterials are lined by certain cells known as juxtablonradar cells or JG cells. These cells release renin. Then this portion that is afferent arterial efferent arterial are in very close contact to the distal tubule. So basically the tubule travels like this and the distal part comes close in contact with this part of the blood vessels. Now this distal tubule has certain cells known as macular denser cells which act as sensors for sodium and chloride. So what happens whenever there is increase in GFR more sodium and chloride reach to this portion. Now these macular denser cells have a transporter sodium potassium to chloride. So they start transporting the sodium and chloride into the cell. Now you know that this transporter acts by secondary active transport. So whenever this transporter is more active there will be utilization of more energy. So ATP will be hydrolyzed and there will be release of a metabolite known as adenosine. Now this adenosine has a role in tubuloglomarapipak. What it does is it is released and acts on the basal portion of these macular denser cells on some receptors known as A1 receptors. This causes release of calcium ions from these macular denser cells which go and act on the afferent arterioles causing the constriction of the afferent arterioles. So what has happened? Increase in venal blood flow cause increased GFR. Again through this tubuloglomarapak mechanism it has lead to constriction of the afferent arterioles. So yes this is a second level of check which is operating. Okay but apart from this there is another mechanism also which is inbuilt in this that this will also affect the release of the venin from these tetraglomerous cells. So increasing venal blood flow increase in GFR will cause decrease in the release of the venin. Now you see this venin is responsible for converting angiotensinogen to angiotensin 1 which is converted to angiotensin 2 by ACE enzyme in the lungs. This angiotensin 2 has multiple effects. Angiotensin 2 basically causes releases of ADH causing increase in thirst. Then it also causes release of aldosterone causes basoconstriction and it causes the constriction of these afferent and efferent arterioles with more effect on this efferent arterioles. So basically by all these mechanisms it is tending to increase blood pressure and by this local effect it will cause increase in GFR right and because effect on efferent arterioles is more. So the blood will be retained in the capillary and the GFR will increase. So if there is decreased release of venin what we have seen in our case these effects will be decreased and hence the GFR will be decreased isn't it? Okay so that's the mechanism of auto regulation of GFR. Myogenic mechanism and the tubular clover feedback which operates by two ways one is adenosine and one is venin. Well thanks for watching the video if you liked it do press the like button share the video with others and don't forget to subscribe to the channel Physiology Open. Thank you.