GFR and Renal BF

Question 1

GFR is regulated by

Answer 1

changing the arteriolar resistance, and systemic BP

Question 2

Kf =

Answer 2

permeability x SA

Question 3

How would hypoalbuminemia change GFR?

Answer 3

decreases the oncotic gc pressure, and increases GFR

Question 4

How would an obstruction of the ureter change GFR?

Answer 4

cause Pbs to increase, and decrease GFR

Question 5

How would vasoconstriction of the afferent arteriole effect GFR and RBF?

Answer 5

same; decreased GFR and RBF

Question 6

How would vasoconstriction of the efferent arteriole effect GFR and RBF?

Answer 6

opposite; increased GFR and decreased RBF

Question 7

How would a hemorrhage and the SNS response effect GFR and RBF?

Answer 7

decrease GFR and decrease RBF, it does this by constricting afferent and efferent arterioles to decrease the amount of Na and H2O filtered and excreted

Question 8

SNS action on arterioles

Answer 8

causes constriction of BOTH afferent and efferent arterioles

Question 9

What stimulates SNS?

Answer 9

Low BP, fear, heavy exercise

Question 10

How does Renin stimulate ANGII

Answer 10

renin is secreted by the JGA cells (can be SNS stimulation) cleaves ANGSN -> ANGI and ACE cleaves into ANGII which binds AT1 receptors

Question 11

Renin is released 3 ways:

Answer 11

baroreceptor detects low pressure in afferent arteriole, Beta-1 agonists (NE and EPI), and stimulation by macula densa (decreased NaCl flow)

Question 12

AngII has a greater effect on the efferent arteriole, it causes

Answer 12

constrict efferent arteriole, raising the filtration fraction, preventing excessive drop in Pgc and GFR (urea excretion maintained)

Question 13

Ang II supports GFR when RPF drops

Answer 13

by constricting the efferent arterioles; but activates the Na and H2O reabsorption in the tubule

Question 14

Ang II effect on tubule

Answer 14

increases Na and H2O reabsorption

Question 15

effects of a Renal a stenosis

Answer 15

decreased Pgc and decreased GFR and decreased RBF; causes Ang II production due to decreased Pgc –> constriction of efferent arteriole to increase GFR

Question 16

NO’s role

Answer 16

to counteract vasoconstriction produced by Ang II and catecholamines (keep RBF from going too low)

Question 17

What stimulates NO?

Answer 17

Shear stress on endothelial cells from constriction, acetylcholine, bradykinin, ATP, histamine

Question 18

Inhibition of NO would result in

Answer 18

increased tonic vasoconstriction by catecholamines and Ang II

Question 19

Link between NO and diabetes and renal failure

Answer 19

diabetes patients have a higher level of NO at the afferent arteriole, this causes excessive vasodilation and results in high Pgc and high GFR. High Pgc over time (glomerular hypertension) causes kidney damage

Question 20

How would an ACE inhibitor help with diabetic glomerular hypertension?

Answer 20

Ang II vasoconstricts the efferent arteriole, if you inhibit Ang II and allow dilation of the efferent arteriole, you can reduce the Pgc and reduce rate of glomerular damage

Question 21

Mechanisms by which Ang II antagonists work

Answer 21

reduce efferent arteriolar constriction, lower Pgc, lower systemic BP, reduce proteinuria, reduce production of cytokines (scarring)

Question 22

PGE2; prostacyclin (PGI2) is a

Answer 22

vasodilator

Question 23

Thromboxane A2; PGF2-alpha is a

Answer 23

vasoconstrictor

Question 24

What stimulates vasodilator prostaglandins

Answer 24

VASOCONSTRICTORS (SNS, renin, decreased ECF, Ang II)

Question 25

Vasodilatory PGs are thought to

Answer 25

counteract vasoconstriction of afferent arterioles to prevent excessive constriction and renal ischemia

Question 26

What would happen in a patient with low GFR and RBF with a high production of Ang II, if they took NSAIDS?

Answer 26

NSAIDS inhibit the production of vasodilatory PG’s, this would further decrease the patient’s GFR and RBF

Question 27

Removal of vasodilatory PGs would cause

Answer 27

constriction of afferent arteriole and further reduced GFR and RBF

Question 28

Bradykinin function

Answer 28

stimulate release of vasodilatory PG and NO to dilate afferent arteriole and increase GFR and RBF

Question 29

What inhibits bradykinin?

Answer 29

ACE, to lower BP, ACE prevents PG and NO, thereby constricting afferent arteriole

Question 30

Autoregulation of GFR and BFR

Answer 30

kidney can avoid changes in GFR and RBF even when systemic BP is fluctuating (eating, exercising, positional changes) Flow is constant despite changes in arteriolar resistance

Question 31

Tubuloglomerular Feedback’s purpose

Answer 31

to modify GFR in order to keep the amount of Na delivered to the distal tubule constant

Question 32

An acute increase in GFR and how the TGF system works

Answer 32

increased GFR and tubular flow changes in NaCl cause constriction of afferent arterioles

Question 33

Mechanism of TGF

Answer 33

macula densa senses high NaCl flow, releases ATP and adenosine (P2X, A1) and stimulate increase in intracellular Ca –> constriction

Question 34

Effects of increased intracellular Ca on Afferent arteriole smooth muscle

Answer 34

causes contraction and prevents the release of Renin

Question 35

How does a protein rich meal effect GFR?

Answer 35

increased protein consumption –> increased aa filtrated –> increased aa reabsorbed which causes increased reabsorption of Na –> macula densa detects low NaCal –> stimulates vasodilation –> increased GFR and RBF

Question 36

Would it be a good or bad idea for a patient with severe kidney disease to eat a high protein diet?

Answer 36

BAD idea; the increased Pgc would cause further damage to the glomeruli