GFR and Renal Blood Flow Overview ch 27

The volume of fluid filtered from the glomerular capillaries into Bowman's capsule per unit time.

The total volume of blood that flows through the kidneys per unit time.

The proportion of plasma that is filtered into the Bowman's capsule. It's calculated as GFR / Renal plasma flow.

Tiny holes in the glomerular capillary walls that allow for filtration of substances from blood.

The layers of the glomerular capillary wall that act as a barrier, preventing the passage of large molecules like proteins.

The negatively charged layer surrounding the glomerular endothelium, repelling negatively charged proteins.

The cells lining the Bowman's capsule with slit pores that allow for filtration.

The process of reabsorbing water and solutes from the renal tubules back into the bloodstream.

The renal pelvis collects urine from the kidneys before it flows into the ureters.

The vasa recta is a network of blood vessels that supply blood to the renal medulla.

Glomerular filtration rate (GFR) is the volume of fluid filtered from blood into Bowman's capsule per unit time.

Glomerular hydrostatic pressure is the pressure exerted by blood within the glomerulus, driving filtration from blood into Bowman's capsule.

The sympathetic nervous system can strongly constrict renal arteries, decreasing renal blood flow and GFR.

Norepinephrine and epinephrine are hormones that constrict blood vessels in the kidneys, reducing GFR and renal blood flow.

Endothelin is a hormone released by damaged blood vessels that can help with blood clotting and also constrict blood vessels in the kidneys.

Angiotensin II is a hormone that constricts the efferent arteriole, increasing glomerular hydrostatic pressure and reducing renal blood flow. This effect helps maintain GFR despite the reduced blood flow.

Nitric oxide (NO) is a vasodilator that helps maintain normal renal blood flow and GFR by relaxing blood vessels in the kidneys.

Autoregulation is the ability of the kidneys to maintain a relatively constant GFR despite changes in arterial blood pressure.

Autoregulation of GFR is crucial for maintaining the normal excretion of water and waste products.

Without autoregulation, even a small increase in blood pressure could drastically increase GFR, leading to excessive urine output and depletion of plasma volume.

Changes in arterial pressure can still have a significant effect on the excretion of water and sodium, even with autoregulation.

A specialized group of cells located in the initial portion of the distal tubule, responsible for sensing changes in sodium chloride concentration and initiating the tubular glomerular feedback mechanism.

The feedback mechanism involving the macula densa and the afferent and efferent arterioles, regulating GFR and renal blood flow.

When a decrease in GFR leads to increased sodium and chloride reabsorption in the loop of Henle, resulting in a lower sodium chloride concentration delivered to the macula densa.

The macula densa, sensing the decreased sodium chloride concentration, triggers two responses: relaxation of the afferent arteriole and renin release.

Relaxation of the afferent arteriole, reducing resistance to blood flow and increasing glomerular hydrostatic pressure.

Renin, released from the juxtaglomerular cells, triggers a cascade that ultimately leads to vasoconstriction of the efferent arteriole.

Constriction of the efferent arteriole, increasing resistance and elevating glomerular hydrostatic pressure, thereby boosting GFR.

The overall effect of the tubular glomerular feedback mechanism is to maintain a relatively constant delivery of sodium chloride to the distal tubule, despite fluctuations in GFR.

The ability of the kidney to regulate its own blood flow and GFR.

The specialized cells in the walls of the initial part of the distal tubule that are directly involved in the tubular glomerular feedback mechanism.

The glomerular filtration barrier, while highly permeable to water, selectively filters molecules based on their size and electrical charge. Smaller molecules like water pass easily, while larger molecules face more resistance. Negatively charged molecules like albumin, even if within the size range, are almost entirely blocked.

The size of the pores in the glomerular membrane is about 8 nanometers. Albumin, despite being only 6 nanometers in size, is barely filtered due to its negative charge. Positively charged molecules are filtered more easily.

The net filtration pressure is the driving force behind glomerular filtration. It's calculated by considering the hydrostatic pressure in the glomerular capillaries and Bowman's capsule, and the colloid osmotic pressure in the capillaries and Bowman's capsule.

Changes in the glomerular capillary filtration coefficient (Kf) can affect the GFR. While Kf is not the primary regulator of GFR, diseases can affect Kf by reducing the number of functioning glomeruli, thus decreasing surface area and GFR.

Increased hydrostatic pressure in Bowman's capsule reduces GFR, while decreased pressure raises GFR. This is not a primary mechanism for regulating GFR, but conditions like urinary tract obstruction can cause increased pressure in Bowman's capsule, significantly affecting filtration.

The colloid osmotic pressure in the glomerular capillaries increases as blood flows through them. This is due to the removal of water during filtration, increasing the concentration of proteins in the blood.

Glomerular filtration rate (GFR) is influenced by both colloid osmotic pressure in the arterial plasma and the filtration fraction. Increasing arterial plasma colloid osmotic pressure reduces GFR, and vice versa.

A decrease in renal plasma flow increases the filtration fraction (percentage of plasma filtered), leading to a rise in colloid osmotic pressure and a decrease in GFR.

Changes in glomerular hydrostatic pressure are the primary means of regulating GFR physiologically. Increased hydrostatic pressure raises GFR. These changes are influenced by arterial pressure, afferent arteriole resistance, and efferent arteriole resistance.

Increased arterial pressure leads to increased glomerular hydrostatic pressure and a rise in GFR. However, other regulatory mechanisms help maintain a stable glomerular hydrostatic pressure despite fluctuations in arterial pressure.

Increased afferent arteriole resistance reduces glomerular hydrostatic pressure and GFR. Conversely, constriction of the efferent arteriole increases resistance to outflow, raising hydrostatic pressure. Severe efferent arteriole constriction can actually reduce GFR due to a greater increase in colloid osmotic pressure compared to capillary hydrostatic pressure.

Constriction of the efferent arteriole has a biphasic effect on GFR. Mild constriction increases filtration by raising hydrostatic pressure, but severe constriction can decrease GFR due to dominant increase in colloid osmotic pressure.

The major segments controlling renal vascular resistance are the interlobular arteries, afferent arterioles, and efferent arterioles. These are regulated by the sympathetic nervous system, hormones, and local internal renal mechanisms.

The renal cortex receives most of the kidney's blood flow. It's the outer portion of the kidney, while the medulla is the inner portion.