Volume Control/Control Of BP

Question 0

Describe how the kidney handles sodium ions in order to change ECF volume

Answer 0

Movement of Na+ = water follows 
PCT - 67% Na, 65% water 
LoH (descending) - 0% Na, 10-15% water
LoH (ascending) - 25% Na, 0% water
DCT - 5% Na, 0% water
Collecting duct - 3% Na, 5-24% water

Question 1

Describe fluid compartments and their electrolyte composition

Answer 1

ECF (plasma, interstitial fluid)

ICF (intracellular fluid)

Question 2

Describe the handling of sodium ions in the PCT

Answer 2

67% of filtered load
Driven by Na+/K+ATPase
Apical membrane channels - Na-H antiporter, Na-glucose symporter, Na-aa cotransporter, Na-Pi

Question 3

Describe the glomerulotubular balance (GT) and the effect on ECF volume

Answer 3

Glomerulotubular balance blunts sodium excretion response to any GFR changes which do occur despite autoregulation

Question 4

Describe sodium ion reabsorption in the loop of Henle (not counter current system)

Answer 4

25% Na in ascending LoH
Na+ ion reabsorption is passive
Epithelium permits passive movement via paracellular movement
NKCC2 in apical membrane (K+ out via ROMK)

Question 5

Describe sodium ion uptake by the early and late distal tubule

Answer 5

Early:
NCC transporter on apical membrane
NCX on basolateral membrane
Calcium reabsorption via PTH
Late:
Principal cells - active reabsorption via ENac on apical membrane
Type B intercalated cells - active reabsorption of chloride

Question 6

Describe how the RAAS regulates sodium ion uptake in response to changes in blood pressure

Answer 6

Decreased blood pressure detected by macula densa cells in DCT
Release of prostaglandins stimulates juxtaglomerular cells to produce renin
Renin + angiotensinogen (from liver cells) –> angiotensin I
Angiotensin I -ACE-> angiotensin II
Angiotensin II –> vasoconstriction, ADH release from pituitary gland, aldosterone increases Na reabsorption

Question 7

Describe the sympathetic control of ADH secretion and the role of the baroreceptor

Answer 7

Sympathetic activity stimulates RAAS
Angiotensin II stimulates ADH release from pituitary gland
Baroreceptors in carotid sinus and aortic arch stimulates baroreceptor reflex which controls acute changes in BP