Lecture 35 4/9/24

Question 1

Which types of control mechanisms are in place around tubular reabsorption?

Answer 1

-nervous
-hormonal
-local

Question 2

What is an important feature of tubular reabsorption?

Answer 2

reabsorption of some solutes can be regulated independently of others, esp. through hormonal control systems

Question 3

What is glomerulotubular balance?

Answer 3

intrinsic ability of the tubules to increase their reabsorption rate in response to increased tubular load

Question 4

Why does the percentage of GFR reabsorbed in the proximal tubule remain constant when filtered load increases?

Answer 4

because rate of reabsorption also increases

Question 5

Besides the proximal tubule, which other segment of the nephron also sees a degree of glomerulotubular balance?

Answer 5

Loop of Henle

Question 6

What is the overall goal of glomerulotubular balance?

Answer 6

prevent overloading of the distal tubular segments when GFR increases

Question 7

Why is it important that glomerulotubular balance and tubuloglomerular feedback work together?

Answer 7

they both work to prevent changes in GFR from dramatically changing urine output

Question 8

What percent of water and solutes is normally reabsorbed?

Answer 8

99%

Question 9

What is the normal rate of peritubular capillary reabsorption?

Answer 9

124 ml/min

Question 10

Which two determinants of peritubular capillary reabsorption are directly influenced by renal hemodynamic changes?

Answer 10

-hydrostatic pressure of the peritubular capillaries
-colloid osmotic pressure of the peritubular capillaries

Question 11

How is peritubular capillary hydrostatic pressure influenced by arterial pressure?

Answer 11

increases in arterial pressure tend to raise peritubular capillary hydrostatic pressure and decrease reabsorption rate

Question 12

How is peritubular capillary hydrostatic pressure influenced by afferent and efferent arteriole resistance?

Answer 12

increased resistance of the afferent or efferent arterioles reduces peritubular capillary hydrostatic pressure and increases reabsorption rate

Question 13

Which factors influence the peritubular capillary oncotic pressure?

Answer 13

-systemic plasma colloid osmotic pressure
-filtration fraction

Question 14

What are the characteristics of filtration fraction?

Answer 14

-the higher the filtration fraction, the greater the fraction of plasma filtered through glomerulus
-protein in the plasma left behind is more concentrated

Question 15

What is filtration fraction?

Answer 15

GFR/RPF

Question 16

How does angiotensin II raise filtration fraction?

Answer 16

by decreasing RPF

Question 17

How do changes in the peritubular capillary physical forces influence tubular reabsorption?

Answer 17

by changing the physical forces in the renal interstitium

Question 18

What is the net movement of water and solutes with the normal, high rate of peritubular capillary reabsorption?

Answer 18

net movement into the peritubular capillaries, with little back leak into the tubule lumen

Question 19

What happens when peritubular capillary reabsorption is reduced?

Answer 19

-increased interstitial fluid hydrostatic pressure
-tendency for greater amounts of solute and water to leak back into tubular lumen
-reduced rate of net reabsorption

Question 20

What is pressure natriuresis?

Answer 20

increased sodium excretion with increased arterial pressure

Question 21

What is pressure diuresis?

Answer 21

increased water excretion with increased arterial pressure

Question 22

Why does urine output increase when systemic blood pressure increases?

Answer 22

-increased GFR
-slight increase in peritubular capillary and hydrostatic pressure
-decreased angiotensin II formation
-internalization of Na transporter

Question 23

What is the site of action for aldosterone?

Answer 23

collecting tubule and duct

Question 24

What are the effects of aldosterone?

Answer 24

-increased NaCl and H2O reabsorption
-increased K+ and H+ secretion

Question 25

What are the sites of action for angiotensin II?

Answer 25

-proximal tubule -thick ascending LOH/distal tubule -collecting tubule

Question 26

What are the effects of angiotensin II?

Answer 26

-increased NaCl and H2O reabsorption -increased H+ secretion

Question 27

What is the site of action for ADH?

Answer 27

distal tubule/collecting tubule and duct

Question 28

What is the effect of ADH?

Answer 28

increased H2O reabsorption

Question 29

What is the site of action for atrial natriuretic peptide?

Answer 29

distal tubule/collecting tubule and duct

Question 30

What is the effect of atrial natriuretic peptide?

Answer 30

decreased NaCl reabsorption

Question 31

What are the sites of action for parathyroid hormone?

Answer 31

-proximal tubule -thick ascending LOH/distal tubule

Question 32

What are the effects of parathyroid hormone?

Answer 32

-decreased PO4- reabsorption -increased Ca++ reabsorption

Question 33

Which mechanisms are used by aldosterone?

Answer 33

-stimulation of Na+/K+ pump -insertion of epithelial sodium channels

Question 34

What are the most important stimuli for aldosterone?

Answer 34

-increased extracellular potassium conc. -increased angiotensin II levels

Question 35

How does aldosterone act on principal cells?

Answer 35

-stimulates Na+/K+ pump -increases Na+ permeability while K+ diffuses out

Question 36

How does aldosterone act on alpha intercalated cells?

Answer 36

stimulates H+ ATPase pumps to increase H+ secretion

Question 37

How does aldosterone act on beta intercalated cells?

Answer 37

stimulates HCO3-/Cl- exchangers to increase HCO3- secretion and Cl- reabsorption

Question 38

What would be seen on a chemistry panel that would indicate Addison's disease/deficit of aldosterone?

Answer 38

-low Na+ -high K+ -Na+/K+ ratio below 27:1

Question 39

What would be seen on a chemistry panel that would indicate hyperadolsteronism?

Answer 39

-high Na+ -low K+

Question 40

When does angiotensin II formation increase?

Answer 40

-low blood pressure -low extracellular fluid volume

Question 41

What are the functions of angiotensin II?

Answer 41

-stimulates aldosterone release -constricts efferent arterioles -directly stimulates Na+ reabsorption

Question 42

What are the angiotensin II mechanisms of action?

Answer 42

-stimulates Na+/K+ ATPase pump -stimulates Na+/H+ exchanger -stimulates Na+/HCO3- co-transporter

Question 43

When is ADH released?

Answer 43

in response to increased extracellular osmolarity

Question 44

What are the mechanisms of action for ADH?

Answer 44

-binds receptors that stimulate cAMP activation of protein kinase A -stimulates movement of aquaporins to luminal membranes -forms channels for water to enter cells

Question 45

What are the two types of diabetes insipidus?

Answer 45

-lacking ADH secretion -defect in renal receptors for ADH

Question 46

When is atrial natriuretic peptide released?

Answer 46

when specific cells of the cardiac atria undergo increased stretch/experience increased blood volume

Question 47

How does ANP act on the body?

Answer 47

-systemic vasodilation -inhibits renin secretion and angiotensin II/aldosterone formation -increases GFR and filtration fraction -increases water excretion and reduces blood volume

Question 48

What are the mechanisms of action for parathyroid hormone?

Answer 48

-increased distal tubular reabsorption of Ca2+ -decreased proximal tubular reabsorption of P -stimulates Mg2+ reabsorption

Question 49

What are the roles of the alpha adrenergic receptors in the kidney?

Answer 49

-alpha1-AR stimulates renal vasoconstriction -alpha2-AR is responsible for Na+ reabsorption

Question 50

What are the roles of the beta adrenergic receptors in the kidney?

Answer 50

-beta1-AR and beta2-AR regulate renal blood flow, GFR, Na+ and H2O reabsorption, acid-base, and renin secretion -beta3-AR regulates renal water and solute reabsorption

Question 51

What happens when the sympathetic nervous system is activated?

Answer 51

-constriction of renal arterioles -reduced GFR and RPF -increased sodium reabsorption -increased renin release and angiotensin II formation