03a: Filtration and Hemodynamics Flashcards
List the layers of the glomerular filtration barrier.
- Single-celled, fenestrated, cap endothelium
- Basement membrane (neg-charged glycoproteins)
- Podocytes (single-celled epithelial visceral layer of Bowman’s capsule)
The size/charge specificity of filtration barrier is due to (X), which cover (Y).
X = neg-charged glycoproteins (nephrin) Y = podocytes, filtration slits, and slit diaphragm
Filtration slit specificity: molecules larger than (X) rejected, smaller than (Y) filtered.
X = 3.6 nm Y = 1 nm
Filtration slit specificity: Intermediate sized molecules with (p/n) charge are better filtered.
Positive (cationic)
T/F: No albumin passes the filtration barrier in glomerulus.
False - small amount may filter through, but partially degraded/reabsorbed
T/F: Albumin normally doesn’t appear in the urine.
True
If kidneys receive 20% CO and Hct is 40%, what’s the RPF?
1 L/min of blood; 60% is plasma, so 600 mL/min is RPF
(X)% of incoming plasma is filtered at the glomerulus. If kidneys receive 20% CO, what can this tell us about GFR?
X = 20;
20% of RPF (which is 600 mL/min if 20% of CO);
So GFR is 120 mL/min
What’s the typical GFR per day? What’s the typical volume of urine excreted per day?
180 L/day;
only 1.8 L/day! (99% water reabsorption)
T/F: Ultrafiltrate has all substances present in plasma at virtually same concentration as in plasma.
Mostly true, EXCEPT proteins
Filtration coefficient is primarily a function of (X), which is increased/decreased by (Y) action of (Z) cells.
X = surface area (permeability) Y = contraction/relaxation Z = podocytes and supporting mesangial cells
T/F: Glomerular capillaries have filtration coefficient that’s 100x smaller than other capillaries.
False - 100x larger
The (hydrostatic/oncotic) pressure in (glom cap/bowman’s space) is virtually zero and ignored.
Oncotic; bowman’s space
GFR is proportional to (X) pressure, which can be defined as:
X = ultrafiltration
[P(GC)-P(BS)]-p(GC)
In glomerular capillaries, what leads to (increase/decrease/constancy) of oncotic pressure as fluid moves from a to e ends?
Increase;
Large filtration of water and retention of proteins
(X) is the only site of minimal reabsorption along the glomerular capillaries.
NONE; no reabsorption here
How much (higher/lower) is hydrostatic P at efferent end of arteriole compared to afferent end? Why?
Virtually the same;
Low resistance to flow in the capillaries
Tubular reabsorption/secretion involve movement of substances across (X). Which paths can be taken?
X = tubular epithelium and capillaries
- Paracellular (between cells)
- Transcellular (through cell)
(X) fraction of Na and (Y) fraction of water filtered at glomerulus is reabsorbed at proximal tubule.
X = Y = 2/3
Most O2 consumed by kidneys is used to:
Energize Na transport (exit across basolateral membrane)
T/F: In tubules, all Na transport is active.
False - luminal absorption of Na is downhill process
Standing Osmotic Gradient Hypothesis: continuous (reabsorption/secretion) of (X) creates small (increase/decrease) of osmolality of (Y) spaces. This leads to:
Reabsorption;
X = Na and Cl
Increase;
Y = intercellular spaces
Drive in reabsorption of water
The Standing Osmotic Gradient Hypothesis primarily describes (X) (reabsorption/secretion) in which part of tubules?
X = water
Reabsorption;
Proximal tubule
T/F: In descending limb, the high permeability to water is due to Standing Osmotic Gradient Hypothesis.
False - due to high osmolality of medullary interstitium
Glucose reabsorption in (X) tubule: its entry is carried out by Na-(dependent/independent) (Y) transporters at (luminal/basolateral) membrane.
X = proximal
Dependent;
Y = SGLT2 and 1
Luminal
SGLT(1/2) is high affinity, low capacity and appears (first/second) in proximal tubule.
SGLT1;
second
Glucose exits tubular cells via (X) method of transport and Na-(dependent/independent) (Y) transporters, located on (luminal/basolateral) membrane.
X = facilitated diffusion
Independent;
Y = GLUT2 and 1
Basolateral
Compared to glom cap’s, peritubular cap pressure is (low/high).
Low
T/F: Constriction of both aff and eff arterioles reduces RBF.
True (increased resistance)
Afferent arteriole dilation (increases/decreases) hydrostatic P in glomerulus. And efferent arteriole dilation?
Increases;
Decreases
T/F: Efferent arteriole constriction to any degree increases GFR.
False- can constrict to degree where reduced RBF compromises filtration
T/F: Both aff and eff arterioles are innervated by sympathetic nerves.
True
RBF and GFR are maintained relatively constant between arterial pressures of which range?
80-180 mmHg
Myogenic response of (aff/eff) arteriole smooth muscle is mediated by (X) channels.
Afferent;
X = stretch-sensitive cation channels
Angiotensin II induces preferential (increase/decrease) in (aff/eff) arteriolar resistance.
Increase;
Efferent
Tubuloglomerular feedback: changes in (X) as a result of (Y) is sensed by (Z).
X = tubular flow rate Y = change in GFR Z = macula densa cells
Tubuloglomerular feedback: increased GFR causes vaso-(constrictor/dilator) secretion by (X) to act on (aff/eff) arterioles.
Vasoconstrictor;
X = macula densa
Afferent
Tubuloglomerular feedback: it’s thought that macula densa sense change in (X), which alters (Y) of cells.
X = NaCl conc in fluid delivered Y = cell volume and/or intracell Ca levels
Tubuloglomerular feedback: high (X) levels sensed by macula densa causes them to secrete (Y), which bind to (Z) receptors on afferent arteriolar smooth muscle.
X = Na Y = Adenosine Z = A1 (recall that A2 receptors cause vasodilation elsewhere)
Tubuloglomerular feedback: the mechanism’s sensitivity is modulated by (X).
X = status of ECF volume
Tubuloglomerular feedback: why would sensitivity by (increased/decreased) at contracted/low ECF volume?
Increased;
Any spontaneous increase in GFR must be dealt with swiftly to prevent life-threatening fluid loss
(Increase/decrease) in blood V and blood P stimulates symp nerve activation and (X) NT release. (X) interacts with (Y) receptors to cause (dilation/constriction) of (aff/eff) arterioles and (increase/reduction) of RBF/GFR.
Increase; X = NE Y = alpha-1 Vasoconstriction; Mainly afferent; reduction
Sympathetic activation of (X) receptors in (Y) cells in (aff/eff) arterioles (stimulates/inhibits) renin release.
X = beta-1
Y = granular
Afferent;
Stimulates
(Increased/decreased) perfusion pressure leads to increased renin production.
Decreased
(NE/renin/AII/ANP) stimulate(s) renal prostaglandin production, which has a (contract/relax) action that dampens (vasodilation/vasoconstriction) effects of (NE/renin/AII/ANP).
NE and AII;
relaxation;
vasoconstriction;
NE and AII
NSAIDs can result in acute (rise/reduction) in (RBF/GFR) because of unopposed (X) due to blockage of (Y).
Reduction; both
X = vasoconstriction
Y = NE/AII stimulation of prostaglandin synthesis
NO is a vasodilator produced by (X) cells and released tonically in renal circulation. (Contraction/expansion) of ECF volume stimulates its release.
X = endothelial and macula densa
Expansion
Levels of dopamine (increases/decreases) with ECF volume expansion. Which effects does this have on GFR/RBF?
Increases;
Vasodilator leading to increase in RBF/GFR
Levels of ANP (increases/decreases) with ECF volume expansion. Which effects does this have on GFR/RBF?
Increases;
Vasodilator (afferent) and vasoconstrictor (efferent) leading to increase GFR with small increase RBF
Glumerulo-tubular balance allows increased (X) of salt and water to be compensated by their (increased/decreased) (Y). This is to avoid:
X = filtration
Increased;
Y = reabsorption
Avoid severe salt/water depletion
List the two mechanisms responsible for glumerulo-tubular balance.
- Starling forces at peritubular cap’s
2. Increased delivery of organic solutes, co-transported with Na
A near constant fraction, (X), of filtered water and salt is reabsorbed at proximal tubule.
X = 2/3
At which tubule does glumerulo-tubule balance take place?
Proximal tubule, loop of henle, and distal tubule
