Lecture 38 Flashcards
what are the 2 factors that determine GFR (glomerular filtration rate)
Net filtration pressure:
Largely controlled by plasma hydrostatic pressure; PH
Glomerular blood pressure (higher than other capillary
pressures)
Filtration coefficient:
Kf; anatomical (same for everyone, constant unless
you develop kidney disease)
Determined by surface area and permeability
GFR = Kf x net filtration pressure
Determinants of Net Filtration Pressure
Glomerular hydrostatic pressure (GHP or PGC): This is the pressure of the blood within the glomerular capillaries. It is the primary force responsible for pushing water and solutes out of the blood and into the glomerular capsule to form the filtrate. GHP is determined by the resistance of the afferent and efferent arterioles, as well as the rate of blood flow.
Bowman’s capsule hydrostatic pressure (BHP or PBS): This is the pressure exerted by the filtrate within the Bowman’s capsule. BHP opposes the filtration process and tends to push fluid back into the capillaries. BHP is determined by the pressure of the fluid in the Bowman’s capsule.
Plasma Protein Osmotic Pressure (πGC): This is the osmotic pressure exerted by the proteins in the blood plasma. (πGC) draws water back into the capillaries from the filtrate, thereby opposing the filtration process. BCOP is determined by the concentration of proteins in the blood plasma.
why is there no osmotic pressure from the Bowman’s space
because you shouldn’t have any proteins in the Bowman’s space
what is the formula for Net filtration pressure
Net filtration pressure (PH) = PGC - PBS - πGC
Why is glomerular filtration rate (GFR) so high?
Large surface area
High blood pressure
Permeable capillaries
Specialized cells
The glomerular filtration rate (GFR) is the volume of fluid filtered by the glomeruli of the kidney per unit time. The normal GFR is approximately 90-120 mL/min in adults, which is much higher than the actual amount of blood flow to the kidneys per unit time. The high GFR is important for maintaining the body’s fluid and electrolyte balance and removing waste products.
How does blood pressure affect GFR?
An increase in MAP leads to an increase in PGC and therefore an increase in PH (net filtration pressure), causing an increase in GFR.
(The high pressure in the glomerular capillaries can also increase the GFR, which can result in increased excretion of water and electrolytes, and decreased reabsorption of essential nutrients, such as glucose and amino acids.)
On the other hand, if the blood pressure is too low, there will be inadequate pressure to drive the filtration process, and the GFR will decrease.
What is the Impact of Vasoconstriction/Vasodilation of the Afferent Arteriole?
The afferent arteriole is a small vessel that supplies blood to the glomerulus, the site of filtration in the kidney. The diameter of the afferent arteriole can be controlled by vasoconstriction or vasodilation, which has a significant impact on the glomerular filtration rate (GFR), the rate at which fluid is filtered through the glomerulus.
Vasoconstriction of the afferent arteriole leads to a decrease in the diameter of the vessel, which reduces blood flow to the glomerulus and decreases the GFR. This occurs in response to a decrease in blood pressure or volume, or in situations where the kidneys need to conserve fluid, such as in dehydration.
vasodilation of the afferent arteriole leads to an increase in the diameter of the vessel, which increases blood flow to the glomerulus and increases the GFR. This occurs in response to an increase in blood pressure or volume, or in situations where the kidneys need to eliminate excess fluid, such as in the case of excess fluid intake
What is the impact of vasoconstriction /vasodilation of the EFFERENT ARTERIOLE?
Vasoconstriction or vasodilation of the efferent arteriole, which is the small vessel that drains blood away from the glomerulus, can also have a significant impact on the glomerular filtration rate (GFR) and kidney function.
Vasoconstriction of the efferent arteriole causes an increase in the resistance to blood flow in the downstream capillaries, leading to an increase in glomerular capillary pressure and a subsequent increase in GFR. This is because blood is being prevented from leaving the glomerulus as easily as it would normally, causing an increase in the pressure inside the glomerulus
vasodilation of the efferent arteriole causes a decrease in the resistance to blood flow in the downstream capillaries, leading to a decrease in glomerular capillary pressure and a subsequent decrease in GFR. This is because blood is being allowed to leave the glomerulus more easily than it would normally, causing a decrease in the pressure inside the glomerulus.
Does GFR always vary with changes in MAP??
if increase MAP–> increase PGC –> increase GFR! (not good)
Implications: dangerous imbalance of fluids, electrolytes, and wastes
We need a regulatory mechanism to maintain a steady GFR
Local Regulatory Mechanisms that Maintain GFR when MAP changes
Myogenic autoregulation: The afferent arterioles in the kidneys have smooth muscle cells that contract or relax in response to changes in blood pressure. When blood pressure rises, the smooth muscle cells of the afferent arteriole contract, causing the diameter of the arteriole to narrow, which helps to maintain the GFR. Conversely, when blood pressure falls, the smooth muscle cells relax, allowing the diameter of the arteriole to increase, which also helps to maintain the GFR.
Juxtaglomerular (tubuloglomerular) (TGF) feedback : This mechanism involves the macula densa cells, which are specialized cells in the wall of the distal tubule of the nephron, and their ability to sense changes in the flow rate and sodium concentration of the tubular fluid. If the flow rate or sodium concentration is too high, the macula densa cells signal the juxtaglomerular cells to release vasoconstrictors, which cause the afferent arterioles to constrict, reducing blood flow and maintaining the GFR.
Juxtaglomerular Apparatus Anatomy
The JGA consists of three main components:
Macula densa (only one that we have to know for this course): A group of specialized epithelial cells in the wall of the DCT that are located adjacent to the glomerulus. The macula densa cells sense changes in the flow rate and sodium concentration of the tubular fluid, and respond by releasing paracrine signals that affect the afferent arteriole.
Juxtaglomerular cells: Smooth muscle cells located in the wall of the afferent arteriole. Juxtaglomerular cells produce and secrete the enzyme renin, which plays a key role in regulating blood pressure and GFR.
Extraglomerular mesangial cells: These cells are located between the afferent arteriole and the DCT. Extraglomerular mesangial cells are thought to play a role in modulating blood flow and GFR by contracting or relaxing in response to changes in blood pressure and volume.
The juxtaglomerular apparatus: Feedback Loop (reduced filtration)
increase GFR –> increase tubule flow –> increase Macula densa secretion (Adenosine) –> Afferent arteriole vasoconstriction –> Decreased glomerular capillary pressure
The juxtaglomerular apparatus: Feedback Loop (increased filtration)
decrease GFR –> decrease tubule flow –> increase Macula densa secretion (Prostaglandin) –> Afferent arteriole vasoconstriction –> increased glomerular capillary pressure
