Glomerular Filtration

1. hydrostatic pressure – forces 1/5 of blood fluid through capillary walls into glomerular capsule

2. filtration membrane – has three parts

• fenestrated capillary endothelium (prevents passage of blood cells)

• basal membrane (allows most solutes but larger proteins)

• visceral layer of glomerular capsule with podocytes and filtration slits

3. solutes that can pass into glomerular capsule

less than 3 nm easily pass (water, sugar, amino acids, nitogenous waste molecules)

9 nm larger proteins cannot pass through

• NFP = force OUT of blood – force to remain IN blood
• NFP = glomerular – (glomerular + capsular )
• hydrostatic osmotic hydrostatic
• pressure pressure pressure
• NFP = 55 mm Hg – ( 30 mm Hg + 15 mm Hg )
• NFP = 55 mm Hg – ( 45 mm Hg )
• NFP = net filtration pressure = 10 mm Hg
• [This is the NET forces pushing fluid/solutes OUT of blood]

1. glomerular filtration rate = milliliters of blood fluid filtered by glomerulus each minute

Factors effecting the GFR:

• total filtration surface area

• membrane permeability to fluid/solutes

• Net Filtration Pressure

2. Normal GFR = 125 ml/min (7.5 L/hr, 180 L/day)

3. NFP – primary factor controlling GFR

• bleeding – NFP drops because of lower glomerular H.P.

• dehydration – NFP drops because of lower glomerular H.P.

1. renal autoregulation – rate of FILTRATE production must be coordinated with systemic blood pressure changes

• myogenic mechanism – circular muscle around the glomerular arterioles reacts to pressure changes

• increased systemic blood pressure -> vasoconstriction of afferent arts.

• decreased systemic blood pressure -> vasodilation of afferent arts.

2. tubuloglomerular feedback mechanism – macula densa cells (of juxtaglomerular apparatus in walls of distal tubules) sense the solute concentration and rate of flow of the FILTRATE

• low filtrate osmolality or flow rate -> vasodilation of afferent arts.

• high filtrate osmolality or flow rate -> vasoconstriction of afferent arts.
3. renin-angiotensin mechanism
• renin (released by juxtoglomerular cells) -> angiotensinogen -> angiotensin I -> (Angiotensin Converting Enzyme (ACE))-> angiotensin II -> global vasoconstrictor (rise in blood pressure) -> aldosterone (reabsorption of more Na+)
• Factors causing release of Renin:

• reduced stretch of juxtaglomerular cells

• stimulation by macula densa cells (as above)

• stimulation of juxtaglomerular cells by sympathetics

1. sympathetics – cause increased release of reninepinephrine – causes increased vasoconstriction

Category: Physiology Notes