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Flashcards in GFR and Renal BF Deck (36):

GFR is regulated by

changing the arteriolar resistance, and systemic BP


Kf =

permeability x SA


How would hypoalbuminemia change GFR?

decreases the oncotic gc pressure, and increases GFR


How would an obstruction of the ureter change GFR?

cause Pbs to increase, and decrease GFR


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

same; decreased GFR and RBF


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

opposite; increased GFR and decreased RBF


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

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


SNS action on arterioles

causes constriction of BOTH afferent and efferent arterioles


What stimulates SNS?

Low BP, fear, heavy exercise


How does Renin stimulate ANGII

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


Renin is released 3 ways:

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


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

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


Ang II supports GFR when RPF drops

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


Ang II effect on tubule

increases Na and H2O reabsorption


effects of a Renal a stenosis

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


NO's role

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


What stimulates NO?

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


Inhibition of NO would result in

increased tonic vasoconstriction by catecholamines and Ang II


Link between NO and diabetes and renal failure

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


How would an ACE inhibitor help with diabetic glomerular hypertension?

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


Mechanisms by which Ang II antagonists work

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


PGE2; prostacyclin (PGI2) is a



Thromboxane A2; PGF2-alpha is a



What stimulates vasodilator prostaglandins

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


Vasodilatory PGs are thought to

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


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

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


Removal of vasodilatory PGs would cause

constriction of afferent arteriole and further reduced GFR and RBF


Bradykinin function

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


What inhibits bradykinin?

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


Autoregulation of GFR and BFR

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


Tubuloglomerular Feedback's purpose

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


An acute increase in GFR and how the TGF system works

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


Mechanism of TGF

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


Effects of increased intracellular Ca on Afferent arteriole smooth muscle

causes contraction and prevents the release of Renin


How does a protein rich meal effect GFR?

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


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

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