Regulation of Extracellular Fluid Volume Flashcards
What is hyovolemia?
How does the body sense hyopvolemia?
What is the body’s response to each of these receptors?
-
Hypovolemia
- decreased effective circulating volume
- Sensed
- Intrarenal baroreceptor-
- afferent arteriole (juxtaglomerular cells)
- release renin
- Cardiopulmonary baroreceptors
- high pressure (carotid sinus & aortic arch)
- low pressure receptors (right atrium & ventricle)
- increase sympathetic output
- Tubuloglomerular feedback (autoregulation
- high distal nephron flow and high NaCl
- macula densa releases adenosine that inhibits renin release & causes afferent arteriolar vasoconstriction that decreases GFR
- low distal nephron flow and low NaCl
- macula densa release NO (and PGE2) that causes afferent arteriolar vasodilation that increases GFR
- high distal nephron flow and high NaCl
- Intrarenal baroreceptor-
What are the actions of angiotensin II?
Major Goal: Restore Effective Circulation Volume
- Vasoconstriction
- Peripheral vessels: increases arterial pressure
- Renal arterioles: constriction of both afferent and efferent arterioles, and decreases renal blood flow and GFR, and reduces excretion of sodium
- Increases Na+ reabsorption
- Proximal tubule: stimulates na-K-ATPase and activity of NHE3 (Na+-H+ exchanger)
- Distal nephron: stimulates Na-Cl co-transport (NCC) and endothelial Na+ channels (ENAC)
- Stimulates aldosterone secretion from adrenal cortex
- Stimulates intake & thirst
- hypothalmic
What are the actions of aldosterone?
How quickly is its onset?
- Stimulates Na+ reabsorption in principal cells; and causes
- K+ secretion (Principal cells)
- Cl- reabsorption (paracellular)
- H+ secretion (intercalated cells)
- Latency is ~90 min (slow)
Aldosterone can increas Na+ by how much?
about 3%
fine control of Na+ excretion
What are the primary stimuli for aldosterone release?
What factors suppress aldosterone release?
- Primary stimuli for release
- Angiotensin II (increases in hypovolemic statess)
- Hyperkalemia - extremely snsitive; direct effect of K+ on zona glomerulosa cells of the adrenal cortex
- Suppressed by (high volume states):
- ANP
- BNP
- Dopamine
How do changes in GFR alter Na+ excretion?
Why?
Na+ reabsorption is dependent on what variable?
- Increase in GFR increases Na+ excretion
- Decrease in GFR decreases Na+ excretion
- Changes in GFR change hte filtered load of Na+ and other solutes that are coupled to Na+ reabsorption
- Na+ reabsorption is load-dependent in the different nephron segments
What is the autoregulatory response when the macula densa senses an increase in flow and an increase in Na+ delivery?
What is the autoregullatory response when the macula densa senses a decrease in flow and a decease in Na+ delivery?
- Increase
- ATP (adenosine) released by Macula Densa
- decreased GFR (maintains normal filtered load)
- decreased renin secretion (allows more Na+ excretion)
- ATP (adenosine) released by Macula Densa
- Decrease
- No & Prostaglandins released by Macula Densa
- increased GFR (maintains normal filtered load)
- increased renin secretion (conserve body Na+)
- No & Prostaglandins released by Macula Densa
What are the responses to a hypovolemic state?
-
GFR
- decrease
-
Sympathetic activity
- increase
-
Angiotensin II
- increase
-
Aldosterone
- increase
-
Prostaglandins
- increase
-
Na+ excretion
- decrease
What are the responses to a hypervolemic state?
-
GFR
- increase
-
ANP & BNP
- increase
-
Urodilatin
- increase
-
Na+ excretion
- increase
What cells release ANP & what is the stimulus to do so?
What are the systemic effects of ANP
- Atrial Natriuetic Peptide (ANP)
- Released by myocytes in the right atria in response to stretch (perceived as hypervolemia)
- Effects
- afferent arteriolar vasodilation (increase GFR and decrease FF)
- decreases peritubular capillary reabsorption
- inhibits Na+ reabsorption (natriuresis) in the collecting tubules, causing diuresis
- inhibits aldosterone secretion
What cells release BNP & what is the stimulus to do so?
What are the systemic effects of BNP?
- Brain (B-type) Natriuetic Peptide
- originally found int he brain
- released from myocytes in the right ventricle in reponse to stretch
- Effects (similar to ANP)
- afferent arteriolar vasodilation (increase GFR and decrease FF)
- decreases peritubular capillary reabsorption
- inhibits Na+ reabsorption (natriuresis) in the collecting tubules, causing diuresis
- inhibits aldosterone secretion
Where is urodilatin produced & what is its function?
- Produced in the distal nephron
- intrinsic renal hormone
- Function
- inhibits Na+ and water reabsorption in medullary collecting duct
- levels show strong correlation with natriuresis (excretion sodium in urine)
Do cortical nephrons or juxtamedullary nephrons have a lower capacity for Na+ and water reabsorption?
Why?
Flow is shunted toward what type of nephron in hypervolemic state? hypovolemic state? Mechanism?
- Cortical nephrons hav ea lower capacity for Na+ and water reabsorption due to shorter loops of Henle
-
Hypervolemic state
- shunted toward cortical nephrons (increases Na+ and H2O excretion)
-
Hypovolemic state
- shunted toward juxtamedullary nephrons (decreases Na+ and H2O excretion)
- Mechanism of shunting: Angionensin II causes greater vasoconstriction in cortical afferent arterioles
What are the effects of norepinephrine and angiotensin II in low volume states?
Net effect?
- Norepinephrin & Angiotensin II
- peripheral vasoconstriction which increases arterial pressure (effective circulating volume)
- stimulate Na+ reabsorption in proximal tubule
- Angiotensin II
- stimulates the Na+- H+ exchanger in the proximal tubule by increasing Na-K-ATPase activity
- stimulate Na+ reabsorption in distal tubule
- Net effect: increased solute & water reabsorption
An increase in arterial pressure has what impact on urine?
This relationship is probably due to what hormone?
- Perfusion pressure dependent natriuresis and diuresis
- increased arterial pressure is correlated with increased urine sodium & volume output
- Intrinsic mechanism: probably involves urodilatin
What are the effects of eating a high Na+ meal?
What about a low Na+ meal?
- High Na+ intake
- “positive Na+ balance”
- Na+ reabsorption is greater than excretion
- water rentention (increased ECBV)
- fluid / weight gain
- “positive Na+ balance”
- Decreased Na+ intake
- “negative Na+ balance”
- Na+ excretion is greater than Na+ reabsorption
- water elimination (decreased ECBV)
- fluid / weight loss
- “negative Na+ balance”
How does the body perceive being immersed in water?
What is the effect on Na+ excretion?
How long does this take?
- Redistribution of the intravascular volume (same as zero G)
- perceived as hypervolemia
- Response
- increase Na+ and water excretion
- long latency (hours)
Why is heart failure perceived as hypovolemia?
- Heart Failure leads to decreased Cardiac Ouptut
- this leads to a decrease in ECBV which the body perceives as hypovolemia & responds with Na+ and water retention
- This Na+ and water retention increases ECBV, which increases venous pressure, caues edema and the ECBV again decreases
- Viscious circle because the pump is not able to maintain the effective circulating blood volume
- The ECBV is perceived as hypovolemia even though extracellular volume is dramatically increased
Why can cirrhosis & Nephrotic syndrome cause edema?
- Cirrhosis (decrease in production of plasma proteins)
- Nephrotic Syndrome (inflammation of glomerular capillaries and loss of protein in urine)
- In both cirrhosis & nephrotic syndrome, there is a decrease in plasma protein concentration, which leads to a decrease in plasma oncotic pressure, so fluid leaves the plasma and enters the interstitial space via osmosis, causing edema
- the movement of water from the plasma to the interstitial space causes a decrease in ECBV, which the body responds to by increasing Na+ and water retention, again diluting the plasma and leading to further edema
Go ahead and draw this out
