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What is Effective circulating volume?
portion of ECF that is effectively perfusing the tissues
What is plasma [Na +] an indication of?
It is NOT an indication of the quantity of sodium in the body but is an indication of body water content
How does the pathway that controls blood pressure lead to a change in sodium concentration?
How do we lose sodium and what can we control?
urine + faeces
The only output that can be regulated is alteration in sodium excretion by the kidneys
Where are baroreceptors found in Low-Pressure Cardiopulmonary Circuit?
Atrial myocytes
Cardiac atria
Right ventricle
Large pulmonary vessels
Where are baroreceptors found in High-Pressure Cardiopulmonary Circuit?
Aortic arch
Carotid sinus
Afferent arterioles of the kidneys (juxtaglomerular apparatus)
What do low and high-pressure zones baroreceptors detect?
low: Changes in effective circulating volume
high: Changes in arterial pressure
What is more important: maintaining ECF or osmolality?
Defence of ECV usually has priority over defence of osmolality
What factors simulate the RAAS system?
Decreased renal perfusion pressure
Increased sympathetic nerve activity (β-adrenergic )
Decreased delivery of NaCl to the macula densa (NaCl sensor)
How does the RAAS system release ANG II?
juxtaglomeular cells sense low bp → release renin
liver makes angiotensinogen
renin convets ANG to ANG I → reaches lungs → lungs release ACE → converts ANG I to ANG II
How does the RAAS system lead to decreased natriuresis and diuresis?
stimulates zona glomerulosa cells (adrenal cortex) → release aldosterone → DCT, thick ascending limb, collecting duct → increases Na+ reabsorption
• Stimulate supraopric nucleus of hypothalamus → release ADH → v2 receptors on collecting duct
• Stimulate hypothalamic thirst centres
• Act on PCT → reabsorption of Na+ and H20
• Stimulates vasoconstriction in blood vessels → increase TPR
How does ANP Increased natriuresis and diuresis
increase in bp is felt in the atria → release ANP
→ increased GFR → more Na+ and water excretion (less reabsorption)
→ inhibit renin secretion → no ANG II → decresed ADH + aldosterone
→ arteriole vasodialation → decreased TPR
How do renal sympathetic nerves decrease natriuresis and diuresis?
decreases GFR
increases renin secretion
increases Na+ reabsorption along the nephron




How does the nephron maintain Constant Na + Delivery to the Distal Tubule in Euvolemia
Autoregulation of the GFR: keeps the filtered amount of Na + constant
Glomerulotubular balance: if GFR increases → amount of Na + reabsorbed by PCT increases proportionately
Load dependence of Na+ reabsorption by the loop of Henle: loop of Henle to can increase its reabsorptive rate in response to increased delivery of Na+
How do we regulate the Distal Tubule and Collecting Duct Na + Reabsorption in Euvolemia?
Aldosterone is the primary regulator of Na + reabsorption by the distal nephron
High aldosterone levels = increased Na + reabsorption (decreased Na + excretion)
Low aldosterone levels = decreased Na + reabsorption (increased Na + excretion)
How does the nephron Control Na+ Excretion with Volume Expansion (hypervolemia)?
less sympathetic activity → GFR increases → increased filtration of Na+
Reabsorption of Na + decreases in proximal tubule and loop of Henle
more Na+ in the DCT → macula densa → less renin + constriction of afferent arteriole → less water reabsorbed → more dilute urine
How does the nephron Control Na+ Excretion with Volume contraction (hypovolemia)?
more sympathetic activity → GFR decreases→ decreased filtration of Na+
Reabsorption of Na + increases in proximal tubule and loop of Henle
less Na+ in the DCT → macula densa → more renin + dialation of afferent arteriole → more water reabsorbed → more concentrated urine
How do we treat extracellular volume expansion?
Treat the underlying cause
Discontinue medications that promote sodium retention (e.g., NSAIDs)
Decrease dietary sodium
diuretics
How do we treat extracellular fluid volume contraction?
Mild: can be corrected orally
Severe: intravenous infusions
usually give normal saline (isotonic)
define oedema
Accumulation of excess fluid within the interstitial space
What causes oedema?
high capillary hydrostatic pressure
increased capillary permeability
reduced plasma oncotic pressure
lymphatic obstruction
renal retention of dietary sodium and water, → expanding the ECF volume
How can the kidney lead to oedema formation when there is myocardial dysfunction?
low bp + CO → low ECV (not ECF) → kidneys retain more Na+ and H20 → increased ECF + blood volume → increase venous hydrostatic pressure → fluid moves into interstitium → oedema
How can we treat oedema?
decrease dietary NaCl intake
Inhibit the kidneys’ ability to retain NaCl: diuretics
Where is Na+ reabsorption adjusted in the nephron in euvolemia?
distal tubule and collecting duct