Flashcards in GFR and Renal BF Deck (36):
GFR is regulated by
changing the arteriolar resistance, and systemic BP
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
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
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