Well, this is interesting. We had four lectures on renal physiology, but the lecture slides are just in one long powerpoint, so I've got to work out where I should divide it up.
In this first post, I will be touching on the anatomy of the kidney as well as the first step in the processing of urine: glomerular filtration.
Anatomy
The urinary system is made up of four main components: kidneys, ureters (which take urine from the kidneys to the bladder), the bladder and the urethra (which takes urine from the bladder out of the body).
The functional unit of the kidney is the nephron. It is made up of a tubular component (where urine is formed) and a vascular component (i.e. the blood vessels surrounding the tubular component). The arrangement of nephrons gives two distinct regions: the renal cortex, which is the outside bit, and the medulla, which form small structures called "pyramids." Nephrons that only dip slightly into the medulla are called cortical nephrons, whereas those that dip fully into the medulla are called juxtamedullary nephrons.
Let's look at the nephron more closely, shall we? Afferent arterioles (from the renal artery) take blood to the glomerulus, from which blood is filtered into the tubular part (more on this in a bit). The arteries then branch out, forming peritubular capillaries (peri = next to), before rejoining to form venules and the renal vein. As for the tubular part, it starts with a cup-shaped bit surrounding the glomerulus known as the Bowman's capsule. This narrows into a proximal tubule, loops around in a Loop of Henle, comes back up as a distal tubule and joins a collecting duct, which then drains into the minor calyces, major calyces, renal pelvis and ureters. From there, urine goes to the bladder to be held before being peed out.
Filtration
The overall process of how stuff works in the kidneys is that lots of blood gets filtered, and then some of the substances in the blood gets reabsorbed. At the same time, some other stuff is being actively secreted into the urine. For now, we're only going to look at the filtration part.
Filtration requires that fluid pass through three main barriers: the glomerular capillary wall, the basement membrane and podocytes. The glomerular capillary wall is a single cell layer, just like every other capillary in the body. The basement membrane is made up of collagen, which maintains structure, and glycoproteins, which are negatively charged and thus repel plasma proteins which are also negatively charged. Podocytes are cells surrounding the glomerulus. They have little "feet," hence their name (podo = foot). The spaces between the "feet" serve as filtration slits that things can pass through. These slits can be opened or closed to allow more or less fluid through.
Now let's look at the main forces affecting filtration! These are very much like the forces affecting capillary filtration (see here). Essentially, the blood pressure inside the glomerular capillaries pushes fluid into the tubules. There is also some hydrostatic pressure from Bowman's capsule, as well as the plasma colloid pressure of the proteins inside the blood (proteins don't get filtered here either). Overall, the net filtration pressure pushes blood out of the capillaries and into the tubules. (This may change in pathologic conditions- for example, a kidney stone could cause the hydrostatic pressure in Bowman's capsule to build up.)
Of these three forces, the first one (glomerular blood pressure) is probably the most readily manipulated. Glomerular blood pressure can be manipulated by changing the radii of the afferent and efferent arterioles. When the afferent arteriole increases in size, more blood goes into the glomerulus, thereby increasing glomerular hydrostatic pressure. (Same thing happens when our overall blood pressure increases.) When the efferent arteriole decreases in size, blood dams up in the glomerulus, also increasing glomerular hydrostatic pressure. And if you're wondering why we don't pee ourselves to death during exercise (due to vasoconstriction of the efferent arteriole and an increase in blood pressure), don't worry, I'll cover that eventually.
Glomerular Filtration Rate
An important parameter to know is glomerular filtration rate, or how much fluid is being filtered at the glomerulus every minute. This depends on net filtration pressure as well as a filtration coefficient Kf, which is determined by factors such as permeability and surface area of the glomerulus. Usually, Kf is around 12.5mL/min. As for net filtration pressure, it's based off three forces as described above: glomerular blood pressure (~55mmHg), plasma-colloid osmotic pressure (~30mmHg) and Bowman's capsule hydrostatic pressure (~15mmHg). As the first force is into the tubules and the latter two are into the glomerulus, the net filtration pressure of fluid into the tubules can be given by 55 - 30 - 15, which is equal to 10mmHg.
Now, glomerular filtration rate can be given by the equation GFR = NFP*Kf. (GFR = Glomerular Filtration Rate, NFP = Net Filtration Pressure). From the numbers above, this gives GFR = 10*12.5 = 125mL/min.
Of course, you don't produce urine at 125mL/min. Our bladders can only hold around 500mL of urine, so if filtration was all there was to it, we'd pee ourselves every four minutes, and rapidly lose a lot of water. Eventually, I'll talk about how reabsorption works to prevent this from happening.
Control of GFR
As I've mentioned, factors such as blood pressure and afferent/efferent arteriole radii can affect glomerular blood pressure, which affect net filtration pressure, which affect GFR. If that was all there was to it, though, we'd produce a lot more urine every time we stood up or exercised, due to the actions of the sympathetic nervous system.
Autoregulation maintains our GFR when our blood pressure is between 80 and 180 mmHg. There are two main mechanisms for this: the myogenic mechanism and juxtaglomerular feedback. The myogenic mechanism works pretty much the same as it does in other areas of the body: increased pressure stretches the arterioles, which respond by constricting. This keeps blood flow to the glomerulus constant despite fluctuations in pressure.
The juxtaglomerular feedback mechanism relies on the macula densa cells of the distal tubule, which, due to the looping around of the nephron, are located very close to the glomerulus (hence juxtaglomerular- juxta = "next to"). An increase in glomerular blood pressure sends more fluid and salts through the tubule. The increased salts are picked up by the macula densa cells, which respond by releasing ATP and adenosine. ATP and adenosine is then picked up by the granular cells of the afferent arteriole, which are basically modified smooth muscle cells that can respond to juxtaglomerular feedback. Hence, ATP and adenosine released by the macula densa results in constriction of the afferent arterioles. When less salt is delivered to the tubules, the macula densa may secrete nitric oxide, which vasodilates the afferent arterioles instead.
Aside from autoregulation mechanisms, the sympathetic nervous system can also regulate GFR. The sympathetic nervous system overrides autoregulation. When blood pressure drops quite low (below around 80mmHg), the sympathetic nervous system kicks in and causes vasoconstriction of the arteries supplying the kidneys. This decreases glomerular blood pressure, which decreases GFR. This is to maintain as much fluid as possible in order to stop blood pressure from falling any more.
Conversely, if you drink so much that your blood pressure increases (you'd actually need to drink a lot), the baroreceptor reflex will kick in, decreasing sympathetic output. This causes vasodilation, increasing GFR.
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