EXAM III Flashcards
What are the components of glomerular filtration and what is the fraction of renal plasma flow that’s filtered?
Water
Ions
Glucose
Urea
0.2 ~ 20%
Filtration fraction = GFR/Renal plasma flow
Molecules w/ (+) charge gets filtered while (-) is repelled and stays in blood; hence why Na+ is mainly the driving force

What are the components that make up the glomerulus?
Podocytes = filtration slits
Pedicelles
Basement membrane
Fenestrated capillaries
What are the layers of the filtration barrier?
Endothelium - w/ fenestrae & (-) charges
Basement membrane - w/ collagen & proteoglycan fibers and strong (-) charges
Podocytes - with (-) charges
What is GFR determined by?
The balance of hydrostatic and colloid osmotic forces acting across capillary membrane (i.e. Starling forces)
The capillary filtration coefficient (which depends on the leakiness of the capillaries and the number and size of pores) K1 - product of permeability and filtering SA of capillaries
Albumin is slightly smaller than filtration pores but have (-) charges
What is the normal GFR?
125 ml/min = 180 L/day
(water has a filterability o = 1.0)
What are the active forces in GFR?
Pg - glomerular hydrostatic pressure
Pb - Bowman’s capsule hydrostatic pressure
πg - glomerular capillary colloid osmotic pressure
πb - Bowman’s capsule colloid osmotic pressure
GFR = K1 x (Pg - Pb - πg + πb)
GFR = K1 x Net filtration pressure
What is K1 and describe how this value alters GFR
Capillary filtration coefficient - product of permeability and filtering SA of capillaries
Hight K1 = high GFR
Low K1 = lower GFR
What are the factors that influence glomerular capillary colloid osmotic pressure? (2)
Arterial plasma colloid osmotic pressure
Filtration fraction (how much blood is actually being filtered)
What are factors that increase glomerular colloid osmotic pressure?
Increasing the filtration fraction
What are the variables that determine glomerular hydrostatic pressure? (3)
Arterial Pressure (pressure going to the glomerulus)
Increases = greater Pg –> increase GFR
Afferent arteriolar resistance
Increase –> less PG –> less GFR
Efferent arteriolar resistance
Increase –> greater PG –> slightly greater GFR
What are the factors that determine renal blood flow?
Renal artery pressure
Renal vein pressure
Total vascular resistance
Renal blood flow = renal art. p-renal vein p./total vasc. resistance
Contains a high rate of Na+ reabsorption, which is related to GFR and rate of Na+ filtered, related to active transport
Kidneys ahve 7x the blood flow of the brain but only 2x O2 consumption
Kidney O2 consumption related to high rate of active Na+ reabsorption
What are the effects of the sympathetic NS on kidneys?
Strong activation:
Constrict renal arterioles
Decrease renal blood flow and GFR
Moderate activation: little effect
What hormones are involved in controlling GFR consistency?
NEpi and Epi (adrenal medulla)
Endothelin
Angiotensin II
Endothelial-derived NO
Prostaglandin and Bradykinin
How does Endothelin work to help control GFR consistency and when is it released?
Released by damaged vascular endothelial cells of the kidneys and other tissues
May contribute to renal vasoconstriction = reduced GFR
May contribute to hemostasis
Plasma levels may increase in toxemia of pregnancy, acute renal failure, and chronic uremia
How does Angiotensin II work to help control GFR consistency?
Increases GFR by constricting efferent arterioles
Usually formed during decreased arterial pressure or volume depleting
Afferent arterioles seem to be protected against the effects of angiotensin II due to NO and prostaglandin release (vasodilators)
How does Nitric Oxide work to help control GFR consistency?
Basic levels helps maintain renal vasodilation
Dervied from endothelial cells
How does Prostaglandins and Bradykinin work to help control GFR consistency?
Vasodilators which may offset effects of sympathetic and angiotensin II vasoconstrictor effects (esp. on afferent arterioles)
Define autoregulation and state its primary function
The relative constancy of GFR and renal blood flow
Primary function = Maintain a relatively constant GFR
Allow precise control of renal excretion of H2o & solutes
Prevent relatively large changes in GFR & renal excretion that would otherwise occur w/ changes in BP
If no autoregulation were to occur in the kidneys, how high can GFR and urine flow increase?
GFR up to 225 L/day (normal 180 L/day)
Urine flow = 46.5 L/day (normal 1.5 L/day)
What is the tubuloglomerular feedback mechanism for autoregulation? What are the components?
Afferent arteriolar feedback mechanism
Efferent arteriolar feedback mechanism
What is the juxtaglomerular complex and where is it?
Next to the glomerulus
Macula dense in distal tubule
Juxtaglomerular cells in afferent & efferent arterioles
(involved in autoregulation)

What is occurring during autoregulation when there is a decrease in GFR, causing a slow rate in loop of Henle? (macula densa)
Increase reabsorption of Na+ and Cl- ions in ascending limb
Decrease NaCl at macula densa
What mechanism occurs during autoregulation when there is a decrease in [NaCl], resulting in a signal from macula densa?
Decrease resistance to blood in afferent arterioles
Increase renin release from JG cells (major storage site of renin)
Increase in angiotensin II
Increase in efferent arteriolr resistance
How must a substance be reabsorbed? What 2 routes can they undergo?
Across tubular epithelial membrane –> renal interstitial fluid –> thru peritubular capillary membrane –> blood
via
Paracelluar (b/w cells) or Transcellular (thru cells) routes via osmosis
Paracellular transport via Ca2+/Mg2+ due to lumen being (+) charged


















