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TUBULAR REABSORPTION Flashcards

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1
Q

autoregulation

A

the ability of the kidneys to modulate blood flow which allows for small fluctuations in blood pressure at rest and at maximum kidney dilation

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2
Q

Hormonal and ANS regulation of blood flow

A

RAAS system, ANP/BNP, SNS, allow for larger more significant changes in blood pressure
- hormonal changes have more long-term effects than ANS

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3
Q

Average renal perfusion range

A

80-180 mmHg

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4
Q

Myogenic hypothesis

A

dictates that when there is an increase in arterial blood pressure, the smooth muscle in arterioles reflexively contracts in response, activating stretch receptors of the afferent arteriole to keep blood flow through the kidneys constant
- afferent arteriole will contract/constrict when it senses increased perfusion pressure or stretch to decrease blood pressure

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5
Q

Tubuloglomerular Feedback

A

mechanism of how the kidneys self regulates itself to maintain homeostasis

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6
Q

Macula densa cells

A

specialized cells of the distal tubule that sense osmolarity of solute passing through the tubule and releases molecules in a paracrine fashion to initiate vasoconstriction (NO, prostaglandins, etc) or vasodilation (adenosine, etc) of the efferent arteriole
- also triggers renin release

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7
Q

How to increase renal blood flow?

A

Dilate afferent arteriole which raises the hydrostatic pressure of the glomerular capillary to increase filtration (GFR)

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8
Q

How to decrease renal blood flow?

A

Constrict afferent arteriole which lowers the hydrostatic pressure of the glomerular capillary to decrease filtration (GFR)

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9
Q

urinary excretion rate

A

the amount of a substance in urine (mg) excreted per minute
- equals concentration of urine x urinary flow rate

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10
Q

filtered load

A

the amount of a solute filtered per unit time
- occurs at the glomerulus, where no transporters are needed to remove solutes from the blood
- equals the concentration of a solute in plasma x GFR

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11
Q

Importance of sodium and sodium reabsorption

A

sodium reabsorption provides the driving force for reabsorption of organic substances like glucose and amino acids, and other ions like bicarb and Cl-
- is also coupled to secretion of K+ and H+

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12
Q

How is sodium transported through apical membrane of tubular cell?

A

by itself via diffusion through Na+ gated channels or via co-transport with other molecules

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13
Q

How is sodium transported through basolateral membrane of tubular cell?

A

pumped into the interstitial space via active transport by Na+/K+ ATPase to enter the peritubular capillaries

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14
Q

proximal tubule

A

site of most water and solute reabsorption

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15
Q

Loop of henle

A

responsible for concentrating and diluting urine

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16
Q

What parts of the nephron are responsible for the fine tuning of filtrate exiting the renal tubules?

A

distal tubule and collecting duct
- are target sites of hormones

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17
Q

Tubular sodium reabsorption

A

almost all sodium filtered is reabsorbed, 2/3 at the proximal tubule

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18
Q

Sodium-hydrogen exchanger (NHE)

A

transporter on the apical membrane of tubular cell that exchanges Na+ for H+ for maintaining acid-base balance and regulating the concentration of Na+ and H+ in the kidney
- this transporter is present on tubular cells throughout the early and late proximal tubule
- is responsible for ~67% of sodium reabsorbed into the blood

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19
Q

Na+/K+ ATPase

A

transporter on the basolateral membrane of tubular cell that moves Na+ out of the cell and K+ into the cell

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20
Q

Sodium-potassium-chloride cotransporter 2 (NKCC2)

A

transporter on the apical membrane of the tubular cell that couples the movement of one Na+, one K+ and two Cl- molecules into the cell
- this transporter is present on the apical membrane of tubular cells in the thick ascending LOH
- is responsible for ~25% of Na+ reabsorbed into the blood

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21
Q

Loop diuretics

A

drugs that block the NKCC2 transporter, inhibiting sodium transport and leading to increased urine volume

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22
Q

Furosemide

A

an NKCC2 inhibitor that blocks the transport protein from bringing NA+, K+ and Cl- into the tubular cell

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23
Q

sodium-chloride cotransporter (NCC)

A

transport protein that moves Na+ and Cl- into the tubular cell at the distal tubule
- is responsible for 4-5% sodium reabsorption at the distal tubule

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24
Q

Epithelial Sodium channel (ENaC)

A

transport protein that moves Na+ into the tubule at the collecting duct, also at distal tubule

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25
Thiazide
an NCC inhibitor that blocks the transport of Na+ and Cl- at the distal tubule
26
Amiloride
an ENaC inhibitor that blocks the transport of Na+ at the collecting duct, sometimes also at distal tubule
27
Aldosterone
stimulates the ENaC transporter to brin in more Na+ to raise blood volume and pressure
28
Diuretics
remove inappropriate or high levels of water d/t edema, hypertension, etc to increase sodium excretion and the urine output
29
Natriuresis
increased sodium excretion
30
Diuresis
increased urine output
31
Electrochemical gradient for Na+ transport
intracellular levels of Na+ are low which favors Na+ entering the tubular cell and the negative electrical potential of the cell favors NA+ entering the cell as well
32
Renal glucose transporters
GLUT and SGLT
33
Where is glucose transported in the kidney
proximal tubule
34
SGLT-1 and SGLT-2
sodium dependent glucose transporters on the apical membrane of the tubular cell - ~90% glucose transported by SGLT-2
35
GLUT1 and GLUT2
sodium dependent glucose transporters on the basolateral membrane that transport glucose ALONE
36
Transport maximum
max rate a substance can be reabsorbed or secreted - once reached, any additional solute remaining is excreted in urine
37
Glucosuria
glucose in urine due to diabetes: insufficient insulin or reduced insulin sensitivity, overwhelmed renal system (hyperglycemia) or defect in glucose reabsorption (renal disease)
38
SGLT2 Inhibitors
lower blood sugar by inhibiting glucose transport back into the blood at the SGLT2 channel, leaving the glucose to exit through urine - FDA warning: know to cause necrotizing fasciitis of the peritoneum
39
Water reabsorption at the Proximal Tubule
isosmotic reabsorption, as almost all water secreted is reabsorbed - reabsorption via paracellular signaling and interactions with tight junctions at the membrane - NOT regulated by ADH
40
Water reabsorption at the Thin Descending LOH
reabsorption is driven by high osmolarity of the medullary interstitium, contributing about 25% of water reabsorption here - interactions with tight junctions at the membrane
41
Water reabsorption at the Thin Ascending LOH
there is NO water reabsorption at the thin ascending LOH
42
Water reabsorption at the distal tubule and collecting duct
Adjustments to final urine output are made here so controlled by aquaporin regulation also target for ADH
43
Aquaporins
special water channel that promote the transcellular transport of water from the renal tubule to the blood - different aquaporins for different parts of the tubule
44
aquaporins at proximal tubule
AQP1 and AQP7
45
aquaporins at collecting duct
AQP2, AQP3, and AQP4 - AQP2 under ADH control
46
aquaporins at descending thin limb
AQP1
47
what aquaporin does ADH act on?
AQP2 to the collecting duct which recruits other aquaporins to reabsorb more water - AP2 brought to apical membrane by cAMP/PKA-mediated transport - recruitment of AQP3 and AQP4 to basolateral membrane
48
Organic cations and anions
Endogenously produced waste products and foreign chemicals that are secreted at the proximal tubule
49
Organic cation transporter
on basolateral membrane of tubular epithelial cell that brings cations into the tubule
50
Transporter promiscuity
the ability of transporters to transport a variety of molecules
51
Organic Anion Transporters
on basolateral membrane of tubular epithelial cells that transport secreted anions in exchange for alpha-keto glutarate - some anions also transported on apical membrane by several transporters including MDR-1 and MRP2 - are also used to transport PAH
52
P-aminohippurate secretion (PAH)
secreted into the tubular cell from the blood via basolateral transporters OAT1 and OAT3 & is secreted into urine via apical transporters MRP2 and NPT1
53
MDR1 and MRP2
transporter on apical membrane of the tubular cell to removes toxins from the body - are both involved in anion excretion
54
Clearance
the rate at which substances are removed from the plasma = volume (ml) of plasma completely cleared of a substance by the kidneys per minute - ALSO = the ratio of urinary excretion to plasma concentration - high clearance= more plasma cleared of the substance - is NOT the same as the excretion rate - is calculated only; most substances are only partially removed in a single pass through the kidney
55
In a 1L of plasma with 10mg of a substance, you determine 1 mg of a substance is excreted in an hour and that 0.L of plasma supplies that 1 mg. What is the clearance?
100ml/hour --> 1.667 ml/min
56
Inulin (lohexol, cystatin C)
primary substance used in determining the GFR - is a fructose polymer not metabolized by the body that is freely filtered by the kidneys and excreted in the urine - exogenous source only
57
Creatinine
by-product of skeletal muscle metabolism that enters the blood at a constant rate proportional to skeletal muscle mass - is generally freely filtered and not reabsorbed except in small amounts at the proximal tubule
58
Creatinine concentration in plasma
very little if any - amount of creatinine in plasma has an inverse relationship with GFR - also depends on body type, changes in diet and consequence of myopathies)
59
Fick Principle
states that the amount of a substance entering the kidney via the renal artery equals the amount of the substance leaving the kidney via the renal vein plus the amount excreted in the urine - one way in, two ways out
60
para-amino hippurate (PAH)
a substance that is both freely filtered and secreted with 90% renal extraction efficacy - is not reabsorbed by the kidneys - amount entering kidneys is amount excreted in urine - carried via OAT - can ignore the amount of PAH leaving through the renal vein
61
Effective Renal Plasma Flow
the volume of plasma flowing through the kidneys per minute - is =to the clearance of PAH since it is not reabsorbed by the kidneys - =220 ml/min
62
Renal blood flow
= renal plasma flow/ (1-hematocrit) = 220 ml/min /(1-0.45) = 400 ml.min - this value is greater than ERPF of PAH because it includes the blood cells contribution as well
63

RENAL PHYS (6 decks)

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