Regulation of Glomerular Filtration Rate – Urine Formation (Nursing)

00:01 The intrinsic controls include renal autoregulation.

00:06 Again, these are going to maintain our nearly constant GFR when the mean arterial pressure(MAP) is in the reign of 80 to 180.

00:17 If we get out of this range, then autoregulation is not going to work.

00:23 There are two types of renal autoregulation.

00:27 We have myogenic mechanisms of autoregulation and tubuloglomerular feedback mechanisms of autoregulation.

00:37 First let's take a closer look at the myogenic mechanisms of autoregulation.

00:43 Local smooth muscles are going to contract when they are stretch.

00:47 And increased blood pressure causes those smooth muscles to stretch and this leads to constriction of the afferent arterioles.

00:57 This constriction of the afferent arterioles then restricts blood flow into the glomerulus.

01:05 This protects our glomeruli from damage that would be due to a high blood pressure.

01:13 A decrease in our blood pressure would cause dilation of our afferent arterioles.

01:20 Both of these are going to help maintain our normal GFR despite the normal fluctuations in our blood pressure and other parts of the body.

01:32 With tubuloglomerular feedback mechanisms of autoregulation.

01:37 There's going to be a flow dependent mechanism that is directed by cells known as the macula densa cells.

01:46 The macula densa cells are a part of the a sending limb of the nephron loop that makes contact with the afferent arteriole of the glomerulus.

01:58 These are going to respond to the filtrate sodium chloride concentrations.

02:05 If the glomerular filtration rate is high, then the filtrate flow rate is also high.

02:12 This will then lead to a decrease in reabsorption time, which means that there's salt concentrations will be higher than normal or higher than what they're supposed to be in the filtrate.

02:26 A feedback mechanism will then cause the constriction of the afferent arteriole, which will then lower the net filtration pressure which will then lower the glomerular filtration rate.

02:39 And this will allow more time for the salt or sodium chloride to be reabsorbed.

02:46 The opposite mechanism occurs when you have a decrease in the glomerular filtration rate, which will lead to a lower sodium chloride concentration than what is expected in the ascending limb of the nephron loop.

03:02 So along with our intrinsic controls, we also have extrinsic controls.

03:07 The purpose of these extrinsic controls is to regulate the glomerular filtration rate in order to maintain systemic blood pressure.

03:19 These extrinsic controls will override the intrinsic controls if our blood volume needs to be increased for any reason.

03:30 Under normal conditions at rest are renal blood vessels are nice and dilated.

03:36 And this is due to the renal auto regulation mechanisms that are taking place at this point are intrinsic controls.

03:45 However, under abnormal conditions such as an extremely low extracellular fluid volume, which leads to a low blood pressure are sympathetic nervous system takes over.

03:58 Norepinephrine it's going to be released by the sympathetic nervous system and epinephrine will be released by cells and the adrenal medulla.

04:08 This will cause a systemic vasoconstriction which will then lead to an increase in our systemic blood pressure.

04:17 This will also cause a constriction of the afferent arterioles which will decrease our glomerular filtration rate.

04:26 These effects will then cause the blood volume and subsequently the blood pressure to increase.

04:34 Another extrinsic control, is the renin-angiotensin-aldosterone mechanism.

04:41 This is actually the main mechanism for increasing blood pressure.

04:46 This involves the release of renin from granular cells.

04:51 Granular cells are cells found in the kidney next and also referred to as juxtaglomerular cells because of their proximity next to the glomerulus.

05:03 These are modified smooth muscle fibers that are going to make up the wall of the afferent arteriole of the glomerulus.

05:12 There are three pathways that leads to the release of renin by the cells.

05:18 Either direct stimulation of the granular cells by the sympathetic nervous system stimulation by activated macula densa cells when the filtrate sodium chloride concentrations are lower than normal, or by reduce stretch of these granular cells.

05:40 So the first intrinsic control is our myogenic autoregulation.

05:46 Let's see how this response to a decrease in our systemic blood pressure.

05:52 If the systemic blood pressure goes down then the blood pressure and the afferent arteriole also is going to go down and also the glomerular filtration rate will be lower than normal.

06:07 Also the stretch of the smooth muscles in the walls of the afferent arteriole also will be decreased.

06:15 We respond to this with vasodilation of the afferent arteriole, which will then increase the glomerular filtration rate.

06:26 The second intrinsic control is are tubuloglomerular autoregulation.

06:33 In response to a decrease in our systemic blood pressure.

06:37 This is going to lead to a decrease in our glomerular filtration rate.

06:43 The filtrate flow and a sodium chloride in the ascending loop will then be lower than normal.

06:51 From there, the macula densa cells of the juxtaglomerular complex of the kidneys will release vasoactive chemicals, which are going to lead to vasodilation of the afferent arteriole.

07:06 This will subsequently caused the glomerular filtration rate to go back up.

07:14 The first extrinsic control is our hormonal control through our renin-angiotensin-aldosterone mechanism.

07:25 In this case, if the systemic blood pressure is lowered then the granulocells of the juxtaglomerular complex are going to release renin.

07:34 This then causes the activation of angiotensin II.

07:40 Angiotensin II can then either cause vasoconstriction and our systemic arterioles, which will then increase our systemic blood pressure or Angiotensin II can also cause this secretion of aldosterone by the adrenal cortex.

07:59 Aldosterone leads to an increase in our sodium reabsorption by the kidney tubules.

08:06 Because of osmosis, water will follow the salt and also be reabsorbed.

08:12 This causes an increase in our blood volume.

08:16 And that increase in our blood volume also causes the systemic blood pressure to go back up.

08:24 The second extrinsic control is our neural controls.

08:28 So in this case when our systemic blood pressure is low.

08:32 This is going to inhibit baroreceptors found in our blood vessels of our systemic circulation.

08:40 This causes the activation of the sympathetic nervous system.

08:45 And from there we get vasoconstriction of the systemic arterioles, which is going to increase peripheral resistance and increase the systemic blood pressure.