 In this video, I will describe the process of glomerular filtration at the renal corpuscle, which is the glomerulus and bowman's capsule, and then describe the intrinsic control of glomerular filtration by the myogenic mechanism and tubular glomerular feedback. This illustration shows us the blood supply to the kidney, of course the kidneys have a rich blood supply because the major function of the kidney producing urine starts with filtration of the blood and filtration occurs at the renal corpuscle. The renal corpuscle is this region here that includes the glomerulus as well as the first segment of the nephron known as the bowman's capsule or the glomerular capsule. But at the renal corpuscle is where blood is filtered by the nephron and in filtration liquid is moving out of the blood and into the nephron into bowman's capsule, the beginning of the nephron. During filtration, a very large amount of the blood fluid moves into the nephron about 125 milliliters per minute in men and a little bit less 105 milliliters per minute on average for women. This would quickly lead to the entire blood volume being removed by the kidneys as urine if there wasn't a process of reabsorption and so the majority of that fluid will be reabsorbed. 99% of the filtrate will be reabsorbed so that only about one to two liters of urine are produced each day. Potocytes are the cells of bowman's capsule that form the inner layer, the visceral layer of bowman's capsule covering the glomerular capillaries. Potocytes are named based on their extensions that are foot-like extensions called pedicles which interdigitate together forming filtration slits. These filtration slits enable liquid from the blood to move into bowman's capsule but the filtration slits are small enough that they prevent any large proteins or any of the formed elements of blood from entering into bowman's capsule. So filtration slits help to create a barrier that only allows small solutes and water to enter the nephron and holds larger particles back in the blood within the glomerular capillary. The glomerular capillary is a fenestrated capillary so it has numerous fenestration pores that enable the bulk flow of liquid from the blood in the glomerular capillary out into the capsular space in bowman's capsule at the beginning of the nephron. Glomerular filtration rate glomerular filtration rate is commonly just abbreviated GFR and GFR glomerular filtration rate is the volume of filtrate produced per minute. So GFR could range from about 80 to 140 milliliters per minute typically a little higher in men than women so on average GFR is around 125 milliliters per minute for men around 105 milliliters per minute for women but you can see there's a range between 80 and 140 milliliters per minute and this is a variable that can be regulated we can increase or decrease the glomerular filtration rate. So filtration at the glomerular capillary is similar to filtration at other capillary beds throughout the body where there's net filtration pressure driving the movement of liquid from the blood out into the extracellular space and in this case for glomerular filtration that liquid moves into the glomerular capsule the bowman's capsule at the beginning of the nephron and becomes the filtrate the first step in the process of urine formation and so the net filtration pressure is the sum of osmotic and hydrostatic pressures we have the blood hydrostatic pressure within the glomerular capillary we can call that the the glomerular blood hydrostatic pressure and so our net filtration pressure equals our glomerular blood hydrostatic pressure minus the blood colloidal osmotic pressure and the capillary hydrates the capsular hydrostatic pressure so the pressure inside bowman's capsule is the capsular hydrostatic pressure CHP and the blood colloidal osmotic pressure is the force of osmosis resulting from the solutes in the blood there's a higher concentration of solute in the blood within the glomerular capillary because large proteins and the formed elements of blood remain in the blood during the process of filtration and so filtrate the liquid being formed in the process of filtration has a lower solute concentration compared to blood therefore the blood colloidal osmotic pressure opposes net filtration pressure similarly the hydrostatic pressure of the filtrate within bowman's capsule the capsular hydrostatic pressure opposes filtration and the primary force that promotes filtration is the glomerular blood hydrostatic pressure so in this example we can see if the glomerular blood hydrostatic pressure is 55 millimeters of mercury and we subtract the 30 millimeters mercury of blood colloidal osmotic pressure and the 15 millimeters of mercury of capsular hydrostatic pressure that's 55 minus 45 gives us a net filtration pressure equal to 10 millimeters of mercury now in order to regulate the glomerular filtration rate we can regulate net filtration pressure by regulating the glomerular blood hydrostatic pressure the blood colloidal osmotic pressure and the capsular hydrostatic pressure are variables that we don't really have a way to easily control however we can easily control the glomerular blood hydrostatic pressure the primary way to do that has to do with regulation of the blood flow in and out of the glomerulus so i'll draw in here the blood vessels the afferent arterial and up here would be the efferent arterial and blood is flowing in through the afferent arterial and out through the efferent arterial so the way that we can increase the glomerular blood hydrostatic pressure is to dilate the afferent arterial as the afferent arterial becomes a larger diameter there's less resistance to blood flow leading to an increase in the glomerular blood hydrostatic pressure similarly if we construct the efferent arterial if the diameter of the efferent arterial becomes more narrow then the rate at which the blood can flow out decreases there's a greater resistance to blood flow through the efferent arterial with constriction of the efferent arterial and that would lead to an increase in the glomerular blood hydrostatic pressure so in contrast we could have constriction of the efferent arterial we could draw we could draw a smaller arterial feeding blood in with greater resistance and we could have dilation of the efferent arterial see if i can erase what i had make it bigger so dilation of this efferent arterial is going to make the resistance to blood flowing out less whereas constriction of the efferent arterial is going to make resistance to blood flowing in greater so constriction of the efferent arterial and dilation of the efferent arterial will lead to a decrease in the glomerular blood hydrostatic pressure and so this is the primary way that we can regulate the glomerular filtration rate is by constricting or dilating the efferent and efferent arterioles to regulate the glomerular blood hydrostatic pressure this illustration shows us the structure of the renal corpuscle with blood entering through the efferent arterial blood flows into the glomerular capillaries where filtration occurs filtration is that liquid moving out of the blood into bowman's capsule liquid from bowman's capsule then flows down into the proximal convoluted tubule and through the rest of the nephron the loop of henley and eventually into the distal convoluted tubule in this illustration the distal convoluted tubule is shown adjacent to the glomerulus and that is enabling communication the macula densa is a region of the distal convoluted tubule that contains sensory receptors monitoring the sodium concentration of filtrate and the flow rate of the filtrate and so the macula densa will secrete paracrine signals to regulate the efferent arterioles the mechanism of tubular glomerular feedback involves the paracrine signal adenosine being released by the macula densa to stimulate the constriction of the smooth muscle surrounding the efferent arterial and this occurs as a mechanism to decrease glomerular filtration rate when the sodium concentration of the distal convoluted tubule becomes too high or the flow rate of the filtrate through the nephron is too high so if the flow rate is too high then there will not be enough time for reabsorption of sodium and the sodium concentration of the distal convoluted tubule will become elevated and this provides a stimulus for tubular glomerular feedback to slow down glomerular filtration rate to stimulate constriction of the efferent arterial so that's one of the mechanisms regulating GFR an intrinsic mechanism called tubular glomerular feedback that is monitoring the concentration of sodium chloride in the distal convoluted tubule and using that variable as information that can be used to regulate glomerular filtration so the myogenic auto regulation mechanism is another intrinsic control mechanism that regulates glomerular filtration rate regulates GFR and this involves the contraction of the efferent arterial smooth muscle in response to stretching as the blood pressure within the efferent arterial increases that will cause stretching of the vascular smooth muscle and stimulate contraction of that vascular smooth muscle so this myogenic auto regulation mechanism helps to stabilize the glomerular blood capillary hydrostatic pressure as any increase in the systemic blood pressure could lead to an increase in the glomerular blood hydrostatic pressure but this is prevented by constriction of the efferent arterial as the blood pressure within the arteries rises the efferent arterial will constrict in order to prevent the glomerular blood hydrostatic pressure from increasing this mechanism helps to stabilize glomerular filtration rate and also helps to prevent damage to the glomerular capillary that could result from high blood pressure myogenic auto regulation is an intrinsic control mechanism that helps to stabilize glomerular filtration rate despite changes in the systemic arterial blood pressure so the arterial blood pressure can be influenced by a wide range of variables but one example would be changing posture as we change posture the pressure within the systemic arteries could change and we don't want that to have an influence on the glomerular filtration rate or the glomerular blood hydrostatic pressure in response to an increase in blood pressure the efferent arterial will stretch and this stretching of the vascular smooth muscle in the efferent arterial stimulates contraction so increasing systemic blood pressure will cause constriction of the efferent arterial leading to a increased resistance in the efferent arterial decreasing the glomerular blood hydrostatic pressure and leading to a resulting decrease in net filtration pressure and glomerular filtration rate the opposite would occur in in response to a low blood pressure there would be dilation of the efferent arterial working to increase the glomerular blood hydrostatic pressure net filtration pressure and glomerular filtration rate so in addition to stabilizing the glomerular filtration rate the myogenic auto-regulation mechanism also works to protect the glomerular capillaries against the damaging effects of high blood pressure if there was too high of a value of the glomerular blood glomerular blood hydrostatic pressure if glomerular blood hydrostatic pressure became too high that could damage the glomerular wall it could lead to damaging of the capillary and so in order to protect the capillary we have this myogenic auto-regulation mechanism that works to stabilize the glomerular blood hydrostatic pressure tubular glomerular feedback is an intrinsic control mechanism regulating GFR and in this mechanism GFR is regulated in order to help stabilize the flow rate of filtrate as well as the sodium concentration of the filtrate so tubular glomerular feedback involves feedback from the distal convoluted tubule to the renal corpuscle to regulate GFR if GFR was too high the flow rate of filtrate through the nephron would be increased and that would lead to an increased flow rate being detected by the macula densa in the distal convoluted tubule similarly an increased flow rate of the filtrate would reduce the amount of time that reabsorption can move sodium chloride out of the filtrate leading to an elevated sodium concentration in the filtrate within the distal convoluted tubule both an elevated flow rate and an elevated sodium concentration can be detected by cells of the macula densa and will stimulate the release of a paracrine signal adenosine then adenosine will bind to receptors on the nearby vascular smooth muscle surrounding the afferent arteriole and adenosine will stimulate constriction of the afferent of the afferent arteriole leading to an increased resistance to blood flow through the afferent arteriole that will lower the glomerular blood hydrostatic pressure leading to a decrease in the net filtration pressure and a resulting decrease in the glomerular filtration rate