Topic 3 - Hemodynamics of Glomerular Filtration Flashcards
Why does RBF exceed the metabolic needs of the kidney?
as an organ that regulates the size and composition of the ECF, it must ‘process’ a large quantity of blood
Why is there a lower partial pressure of oxygen in the outer and inner medulla compared to the cortex?
cortex provides lots of flow for filtration and reabsorption
in medulla:
- higher flow would wash out the osmotic gradient
- lower flow would increase the risk of papillary necrosis
What does it mean to have localization of renal vascular resistance (afferent and efferent arterioles)?
pressure profile
- renal a (100mmHg) -> glomerulus (50mmHg) -> renal v (12mmHg)
implications:
- high resistance sites as points of regulation
- afferent and efferent arterioles
- spatial separation of filtration and reabsorption sites
- two arteriole segments and two capilarry beds on either side
- at glomerulus: site strict for filtration
- at peritubular: site strict for uptake or reabsorption
- two arteriole segments and two capilarry beds on either side
Compare efferent and afferent artiole resistances
equal resistances:
- renal arteriole pressure = 100
- GFR = 20%
- Pgc = 60
- Peritubular cap pressure = 20
- Filtration fraction (FF) = GFR/RPF
increased afferent resistance:
- renal arteriole pressure = 100
- GFR = decreased;
- Pgc = 40
- peritubular cap pressure = 13
- FF = decreased GFR/decreasd RPF -> same FF = 20%
increased efferent resistance
- renal arteriole pressure = 100
- GFR = 70
- Pgc = 70
- peritubular cap pressure = 30
- increase FF = increase GFR/decrease RPF -> increased FF = 30%
What is net filtration pressure?
the algebraic sum of the magnitude of direction of forces of the glomerular capillary pressure and Bowman’s capsule hydrostatic pressure
hydrostatic pressure gradient
- glomerular capillary hydrostatic pressure (Pgc)
- Bowman’s space hydrostatic pressure (Pbs)
colloid osmotic (oncotic) pressure gradient
- glomerular capillary oncotic pressure (∏gc)
- Bowman’s space oncotic pressure (∏bs)
Pgc = 60mmHg
Pbs = -15mmHg
∏bs = -29mmHg
Net: 26mmHg
What is the filtration coefficient (Kf)?
Kf is a factor that accounts for surface area and the conductance of water
What are the dynamics of glomerular filtration?

What is the glomerular ultrafiltration equation?
GFR is the result of the same forces that cause filtration across any capillary wall
GFR = Kf * [(Pgc - Pbs) - (∏gc - ∏bs)]
Kf = glomerular ultrafiltration coefficient
- in disease states, Kf is often reduced either as a result of reduced area for filtration of individual glomerular capillaries or because of reduction in number of nephrons
How do changes in glomerular ultrafiltration equation predict changes in GFR?
glomerular hydrostatic pressure (Pgc)
- afferent arteriole resistance
- constriction -> decrease glomerular pressure
- dilation -> increase glomerular pressure
- efferent arteriole resistance
- constriction -> increase glomerular pressure
- dilation -> decrease glomerular pressure
- tubular pressure (Pbs)
- obstruction -> increase pressure in Bowman’s space -> decrease net filtration and decrease GFR
- colloid osmotic (aka oncotic) pressure (∏gc)
- hyper- or hypoalbuminemia
- hyper -> decrease GFR
- hypo -> increase GFR
- hyper- or hypoalbuminemia
- filtration coefficient (Kf)
- pathological damage to the glomerular membrane (permeability and/or area)
What is a reduction in GFR in disease states most often due to?
decreases in the ultrafiltration coefficient (Kf) because of loss of filtration surface area
GFR also changes in pathologic conditions because of changes in the hydrostatic pressure in the glomerular capillary (Pgc), oncotic pressure in the glomerular capillary, and hydrostatic pressure in Bowman’s space (Pbs)
How do changes in Kf affect GFR?
increased Kf -> increased GFR
- some drugs and hormones that dilate the glomerular arterioles also increase the Kf
decreased Kf -> decreased GFR
- some kidney diseases reduce the Kf by decreasing the number of filtering glomeruli (i.e. diminished surface area)
- drugs and hormones that constrict the glomerular arterioles decrease Kf
How do changes in Pgc affect GFR?
decreased renal perfusion -> decreased GFR because Pgc decreases
- reduction in Pgc is caused by
- a decline in renal arterial pressure
- an increase in afferent arteriolar resistance
- a decrease in efferent arteriolar resistance
How do changes in ∏gc affect GFR?
an inverse relationship exists between the ∏gc and the GFR
- alterations in the ∏gc result from changes in protein synthesis outside the kidneys
- protein loss in the urine caused by some renal diseases can lead to a decrease in the plasma protein concentration and thus a decrease in the ∏gc
How do changes in the Pbs affect GFR?
an increased Pbs reduces the GFR
- acute obstruction of the urinary tract (e.g. a kidney stone occluding the ureter) increases the Pbs
decreased Pbs enhances the GFR
A decrease in GFR but no change in FF is due to?
change in afferent arteriole resistance
A decrease in GFR and an increase in FF is due to
predominant effect on efferent side
How are GFR and RBF regulated?
intrinsic regulation - autoregulation
- over a wide range of blood pressure (80-190), the renal blood flow and glomerular filtration rate are relatively constant
- despite this change in pressure, adjustments are made to keep renal blood flow and the GFR constant
How is GFR and RBF regulated over a wide range of arterial blood pressure?
the fact that both GFR and RBF are autoregulated (i.e. no change in filtration fraction[FF]), indicate that the resistance changes that maintain this constancy is occurring in the afferent arteriole
How does autoregulation occur?
every single nephron has its distal tubule return back to the glomerulus origin - feedback signal
- increase in GFR = more fluid will be filtered in the tubule
- increase in NaCl delivery to the loop of Henle
- more NaCl delivered, more is generated; more fluid and more NaCl
- arrive at macula densa segment and generates a signal by the juxtaglomerular apparatus
What are some main features of tubuloglomerular (TG) feedback?
increase delivery of Na+ to loop of Henle causes more Na+ to be reabsorbed, utilizing ATP for active transport
- hydrolysis of ATP for transport energy, forms ADP, AMP, and adenosine
adenosine acts to constrict the afferent arteriole and reduce GFR towards normal
- adenosine associated with the increase transport, sends a signal, causes constriction of the afferent arteriole, which brings back GFR to the control level
What happens in the juxtaglomerular apparatus?
made up of granular cells containing renin
- increase delivery of NaCl
- NaCl pumped across macula densa cell utilizing ATP
- formation, the hydrolysis of ATP leads to formation of adenosine
- adenosine is released and causes a vasoconstriction of the juxtaglomerular cells (and increase renin release)
How is the renal autoregulated extrinsically via the renin-angiotensin system (RAS)?
Angiotensin II - constricts both afferent and efferent arteriole, but predominates on the afferent arteriole
- Ang II has an overall effect to minimize renal blood fluid and sodium losses and to maintain arterial blood pressure
- exerts powerful renal vascular effects, which elicit decreases in RBF and to a lesser degree in GFR
- usually an increase in filtration fraction
- ACE inhibitors block the effect on the efferent arteriole and often result in a decrease in GFR
How is the renal autoregulated extrinsically via endothelial factors?
Nitric oxide - vasodilates both afferent and efferent arteriole
- endothelial cells respond to various physical stimuli (shear stress) and hormonal agents (e.g. thrombin, bradykinin) to release vasoactive factors
- NO is formed constitutively and diffuses out of the cell into adjoining cells
- through stimulation of soluble guanylate cyclase and increased cGMP levels in smooth muscle cell, NO exerts powerful vasodilator actions
How is the renal autoregulated extrinsically via paracrine factors?
Prostaglandins - vasodilation of afferent and efferent arterioles
- while prostaglandins are not major determinants of resting renal vascular tone under normal states of hydration and sodium balance, they do exert protective effects in response to vasoconstrictor stimuli, hypovolemic states, or hypotensive episodes
- when the kidney is under the sustained influence of vasoconstrictor stimuli such as elevated catecholamine levels, increased renal nerve activation, and increased activity of the renin angiotensin system, activation of the PG production helps counteract the vasoconstrictive effects of these stimuli