• filtrates is Free of blood cells & proteins

• modified passing through nephron
• free passage of water, small solutes (glucose, aa, electrolytes)

1.  Fenstrated capillary endothelium- permeable to water & dissolved solutes
2. Glomerular basement membrane- collagen, glycoproteins contain anionic charges
3. Podocyte epithelium- slit pores b/w podocytes restricts large molecules

• cations- flow the fastest w/respects to comparative radius size
• neutral
• anions- remember that on Glomerular BM the proteins contain anionic charges (repel)

1. hydraulic permeability- of glomerular mem
2. Surface Area for filtration

--> product of 1 & 2= ultrafiltration coefficient Kf

3. Capillary ultrafiltration pressure (UP)-driving force, determined by hydrostatic & colloid osmotic pressures in glomerular cap

GFR= Kf * UP

Mechanisms for altering GFR

(GFR= Kf * UP)

• Altered Kf: mesangial cell contraction, located w/in glomerular capillary loops, contraction shortens the loop, lowers Kf 
• Altered UP: changesin Pgc (pressure in glom capillary)
• Pgc determined by 3 factors:

- renal arterial BP

- afferent arteriolar resistance

-efferent arteriolar resistance

• greater prssure drop upstream of glom. cap
• Pgc falls (lowers GFR)
• Renal blood flow falls (due to increased resistance)
• Pressure rises before and drops afterwards (include peritubular cap P)

* see slides 25, 26, 27 

• pooling of blood in glomerular capillaries
• increased Pgc (increases GFR)
• pressure drops downstream (includes peritubular cap P) 
• affects on renal blood flow:

- severe blood becomes stagnant (GRF drops)

- moderate, will increase GFR

* see slides 25, 26, 27 

1. Myogenic- response to increased systemic arterial P , intrinsic property of vascular smooth musc to resist stretch (stretch causes contraction-> narrowing of vessels, decreased R, RBF, GFR)
2. Tubuloglomerular feedback-involves the juxtaglomerular apparatus (JGA) responds to:

• increased GFR (w/increased BP, the Macula densa senses the increase in fluid deliver to prod vasoconstrictors to decrease fluid)
• decreased GFR (w/decreased renal BP, less Na, Cl filtered & delivered to MD, MD signals granular cells to secrete renin to produce angiotensin II)

• Macula densa- in end wall of thick ascending limb of Henle's loop
• Extraglomerular mesangial cells (AKA lacis cells)- communicates info from the MD to the smooth musc of the afferent arterioles
• juxtaglomerular (granular) cells - in afferent & efferent arteriole smooth musc

• released in response to renin release by the MD due to decreased GFR
• it is a potent vasoconstrictor to restore the BP
• efferent arteriolar vasoconstrition:

- moderate causes minimizes fall in GFR

-severe GFR falls due to stagnant blood flow

• released by endothelial cells
• causes smooth musc vasodilation
• dampens the vasoconstriction by angiotensin II & SNS
• why is this important?

• constriction of afferent (lesser extent efferent) arterioles to decrease RBF & GFR
• increase renin secretion by granular cells, which stimulates angiotensin II products to cause arteriolar constriction to raise BP and my stabilize GFR (if moderate degree)