L2 RBF and GFR Flashcards

1
Q

Characteristics of RBF

A

Kidneys receive 1/4th of CO
High flow not needed for metabolism
Needed to support filtration (20% of plasma is filtered)

180L of filtrate formed per day

Entire plasma volume filtered 65 times per day
If everything filtered lost, would lose entire plasma volume in <30min
Must reabsorb a lot

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2
Q

Vasoconstrictors

A

Sympathetic nerves:
Vasoconstriction via alpha1 receptors
decrease RBF & GFR

Angiotensin II, ADH, ATP, endothelin- decrease RBF & GFR

AT II- constricts both afferent and efferent arterioles but efferent is more sensitive at lower concentrations of AT II- increase GFR and decrease RBF

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3
Q

Vasodilators

A

Atrial natriuretic peptide (ANP), glucocorticoids, NO, prostaglandins (PGE2, PGI2)

Increase RBF & GFR

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4
Q

Autoregulation of RBF and GFR

A

Constant blood flow and GFR through a range of arterial pressures

Pressure range 80-180mmHg

During severe blood loss, decreased RBF and GFR will occur due to hypotension

If arterial pressure > 180 both RBF and GFR will increase proportionally

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5
Q

Two mechanisms of autoregulation

A

Myogenic mechanism

Tubuloglomerular feedback (flow-dependent)

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6
Q

Myogenic mechanism

A

Intrinsic to VSMC

Contract in response to stretch

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7
Q

Tubuloglomerular feedback

A

Flow dependent

Increasing GFR increases NaCl delivery to LOH

sensed by the macula densa which causes resistance of the afferent arteriole (RA) to increase thereby decreasing RBF & GFR

defends RBF & GFR by changing resistance of afferent arteriole

Maintains constancy of salt load delivered to distal tubule

Signal unidentified, may be thromboxane, ATP, or adenosine

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8
Q

Nature of filtrate

A

Protein does not normally pass the filter in significant quantities

All small MW solutes that are not protein bound appear in the filtrate in the same concentrations as in blood plasma

Fluid in bowmans capsule is essentially a protein free filtrate of blood plasma

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9
Q

Route of filtrate

A

Fenestrae, basal lamina, filtration slits between pedicels of podocytes

Filtration slits bridged by diaphragms

Substances separated by size (7000 easy, 70000no) and electrical charge (basal lamina and slits coated with - charges) proteins usually have a - charge and are repelled

Basal lamina and filtration slits are main barriers to proteins

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10
Q

Permeability based on charge

A

Polycation will filter more readily than neutral (control) and polyanion

Filter ability decreases with size

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11
Q

Capillary filtration coefficient

Kf

A

Filtration rate (ml/min/mmHg) produced by each mmHg of net filtration pressure

Glomerular capillary Kf May be 7-15

Kf for glomerular capillaries is 50-100 greater than capillaries in muscle or skin

Can be altered by mesangial cell (all reduces Kf)

Use to calc GFR

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12
Q

Net filtration pressure

NFP

A

PGC- blood pressure in glomerular capillary- driving force for GFR

PBC- back pressure in Bowmans capsule, reduces GFR

OncoticGC- oncotic pressure of glomerular capillary blood, due to proteins unable to cross barrier, retards GFR, increases as plasma diverted into BC

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13
Q

P GC

A

Blood pressure in glomerular capillary

Driving force for GFR

Remains constant at afferent and efferent arteriole ends because outlet is an arteriole and arterioles are resistance vessels

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14
Q

P BC

A

Back pressure in bowmans capsule

Reduces GFR

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15
Q

Oncotic GC

A

Oncotic pressure of glomerular capillary blood

Due to protein unable to cross barrier

Retards GFR

Increases as plasma diverted into BC

Increases from afferent to efferent arteriole end because moving fluid but proteins don’t move, they’re confined to inter vascular space

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16
Q

Increase P GC

A

Increase GFR

17
Q

Decrease P GC

A

Decrease GFR

18
Q

NSAIDs block effects of prostaglandins

A

PGE2 and PGI2 produces locally in kidney in response to SNS stimulation of vascular smooth muscle in afferent arteriole and high levels of circulating AT II

both vasodilate the afferent arteriole reducing vasoconstriction production by SNS stimulation to maintain blood flow

NSAIDs inhibit synthesis of prostaglandins
Which inhibit activity of COX 1 and 2 and interfere with the protective effects of prostaglandins on RBF