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Physiology Renal Quiz 2 > ECFV > Flashcards

ECFV Flashcards

1
Q

How do KD play a central role in this process by regulating the volume of ECFV?

A

• plasma volume via changes in ECFV and RBC volume via erythropoietin.

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2
Q

How is the ratio of the two subcompartments of ECF (i.e. the interstitial fluid and blood plasma) determined by the Starling forces?

A
  • If blood volume is high, capillary pressure increases and fluid is filtered out from the plasma into the interstitium.
  • If blood volume declines, fluid is driven into the blood from the interstitium by the negative oncotic pressure.
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3
Q

What is the clinical relevance of the KD and blood pressure?

A
  • The kidneys play an overriding role in regulating BP.

* Treatment of hypertension is directed at renal handling of NaCl.

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4
Q

What are the three routes of Na loss?

A
  • The typical daily intake of Na on a Western diet is ~120 mEq.
  • Na (~90%) is excreted via the kidneys, ~7% by the feces and ~3% through the skin.
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5
Q

Do the KD have a role in Na conservation of the GI and skin?

A
  • With low Na intake, in addition to renal Na conservation, Na loss via the GI tract and the skin must be also curtailed.
  • Interestingly, the signals that control these latter routes of Na loss, also originate from the kidney.
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6
Q

What governs salt appetite?

A
  • Na appetite, which is analogous to the mechanism of thirst.
  • The signals that govern salt appetite also emanate from the kidney.
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7
Q

Although regulation of ECFV is critical for the regulation of blood pressure, it is not ECFV as a whole that is sensed and regulated.

A

• All receptors that govern Na balance, and thus ECFV, reside in the circulatory system.
• They fall into two main categories
o high-pressure receptors
o low-pressure receptors.

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8
Q

Where do the dominant High Pressure Receptors reside?

A
  • The dominant high-pressure receptors are in the afferent arterioles in the kidney.
  • The high-pressure receptors in the carotid sinus and aortic arch play a minor role.
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9
Q

Why do high pressure receptors in the carotid sinus and aortic arch play only a minor role?

A

• The role of the carotid sinus and aortic arch receptors is the short-term control of blood pressure, and to protect the brain from ischemia.
• baroreceptors in large arteries adapt to a continuous increase in arterial pressure (i.e. hypertension) within a few days.
o The essence of this adaptation is the thickening of arteries by the proliferation of smooth muscle cells and the incorporation of more connective tissue. Due to this anatomical restructuring, the increase in wall tension (which is the stimulus for the baroreceptors) is transient.

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10
Q

Why are the renal afferent arterioles the dominant high-pressure receptors?

A
  • Vessel restructuring does not occur in the afferent arterioles as they are composed of a single layer of muscle cells, even in hypertensive states.
  • The renin-producing granular cells at this site lack contractile fibers, and therefore always experience a stretch that is proportional to the actual blood pressure.
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11
Q

Why do we need low pressure receptors? Where are they located?

A
  • Low-pressure receptors are important for the intermediate-term (hours) regulation of blood pressure.
  • These receptors reside in the cardiac atria, the vena cava and large pulmonary vessels.
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12
Q

Why do low-pressure receptors show the greatest response to ECF volume changes?

A

• Since these structures are much more distensible and most of the blood resides at the low-pressure end of the circulation, low-pressure receptors show the greatest response to changes in blood volume.

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13
Q

Why is a dual regulation by high- and low-pressure receptors is necessary?
What is “Effective Circulating Volume” ?

A

• A dual regulation by high- and low-pressure receptors is necessary, because blood pressure is not only dependent on the total volume of blood but also on its the distribution within the vasculature.
o In upright position a significant portion of the blood pools in the lower extremities and therefore not available for perfusing tissues.
o The total blood volume minus this un-measurable amount of pooled blood that circulates sluggishly is termed “effective circulating volume”.

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14
Q

Thought Question. Explain how low-pressure receptors effect Na excretion when a person is immersed in a pool of water? Why aren’t high-pressure receptors involved?

A
  • This is a case of “effective circulating volume”
  • outside hydrostatic pressure compresses the extremity blood vessels thereby increasing the amount of blood in the thorax.
  • Since water immersion results in a substantial increase in renal Na excretion without a change in arterial pressure, the natriuresis is mediated solely by stimulation of low-pressure receptors in the thorax.
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15
Q

Thought Question. Why would heart failure stimulate renal Na retention?

A
  • Congestive heart failure is associated with avid renal Na reabsorption in spite of a significant increase in venous pressure.
  • During prolonged increase in venous pressure, low-pressure receptors are reset by a mechanism similar to that described above for high-pressure receptors and therefore do not signal to excrete Na.
  • At the same time, as a consequence of the failing heart, renal arteriolar pressure is reduced, which generates signals that increase Na reabsorption (and edema).
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16
Q

What are the main mechanisms for Na reabsorption?

A
  • Renin-Angiotensin-Aldosterone System (RAAS)

* And activation of the renal sympathetic nerves.

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17
Q

What is the main inhibitor of Na reabsorption?

A

• Atrial Natriuretic Peptide (ANP).

With changes in effective circulating volume, the kidney makes appropriate adjustments in Na excretion. Low- and high-pressure receptors regulate renal Na reabsorption by altering the balance between natriuretic and anti-natriuretic mechanisms.

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18
Q

What is the sequence of the RAAS system? Where is each enzyme/hormone produced?

A
  • The RAAS dwarfs all other Na balance mechanisms.
  • renin, is a proteolytic enzyme produced by the granular cells of the afferent arterioles.
  • renin cleaves angiotensinogen, a circulating protein produced by the liver to generate Angiotensin I (AI)
  • AI itself is biologically inactive.
  • It is converted into the biologically active form, Angiotensin II (AII), by further proteolysis catalyzed by Angiotensin Converting Enzyme or ACE.
  • ACE is an ectoenzyme that is expressed on the surface of most endothelial cells.
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19
Q

How does AII facilitates Na retention?

A

• AII facilitates Na retention by several synergistic mechanisms that include both renal and extrarenal actions.

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20
Q

What are the main renal effects of AII?

A

• AII directly stimulates Na reabsorption in the proximal tubule by increasing the activity of the apical Na/H exchanger.
• AII also enhances renal Na conservation by affecting several aspects of renal hemodynamics:
o a) It lowers the set point and heightens the sensitivity of the TGF, and thus an increase in NaCl load delivered to the macula densa will trigger a more robust decrease in GFR.
o b) By constricting the efferent arterioles, AII tilts the peritubular Starling forces in favor of reabsorption by the proximal tubule (decreased hydrostatic & increased oncotic pressure).
• Students are occasionally confused by the consequences of AII-mediated efferent constriction, since such an effect by itself would tend to increase GFR, which seems counterproductive.
• Keep in mind that AII levels increase only when blood pressure declines, and thus, this effect helps to preserve GFR rather than increasing it.
o c) AII also reduces medullary blood flow, which in turn enhances urinary concentrating ability and increases Na+ reabsorption in the thin ascending limb of the loop of Henle.

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21
Q

What is the main extrarenal (and most important) effect of AII? What are secondary effects?

A

• The main effect is stimulation of aldosterone
• Secondary: AII is a very potent vasoconstrictor because its direct effects on vascular smooth muscle are amplified by several indirect mechanisms.
o These include increased sympathetic activity, diminished vagal tone and baroreflex sensitivity, enhanced norepinephrine release and reduced reuptake at sympathetic terminals
• Secondary: AII stimulates thirst, and (to a lesser degree) Na appetite.

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22
Q

What is aldosterone and where it produced (be specific)? What are the receptors that Aldosterone binds to? How is the Aldosterone receptor different than AII and other peptide hormone receptors?

A
  • Aldosterone is a steroid hormone produced by the outer layer (zona glomerulosa) of the adrenal gland.
  • Its effects are mediated by the mineralocorticoid ¬receptor (MR).
  • Unlike receptors for peptide hormones such as AII, the MR is intracellular and functions as hormone-activated transcription factor.
23
Q

How does Aldosterone-mediated Na conservation affect all facets of maintaining Na homeostasis?

A

• It is the main stimulator of Na reabsorption in distal tubules and collecting ducts, and thus, the final arbiter of renal Na excretion.
• Enhances Na absorption in the colon and sweat glands, minimizing extrarenal Na loss.
• Aldosterone is also the main driver of Na intake through appetite.
o It acts on the CNS to stimulate salt appetite and increases the sensitivity of taste buds to salt.
o In addition, aldosterone reduces salivary Na concentration thereby lowering the threshold for Na sensing.

24
Q

What is ENaC? How does aldosterone affect apical ENaC? How does aldosterone effect basolateral Na/K-ATPase?

A
  • Epithelial Na channel (ENaC) (Aldosterone target)
  • In collecting duct, ENaC resides in the luminal membrane and is the route of Na+ entry into the cell.
  • rate-limiting step in Na reabsorption
  • Besides stimulating ENaC expression, aldosterone also increases the synthesis of the basolateral Na/K-ATPase.
25
Q

How effective is the ENaC Na/K combo at reabsorbing Na?

A

• Since Na+ uptake into the cell proceeds downhill a steep electrochemical gradient (low intracellular [Na] and negative potential inside the cell), this mechanism can remove practically all Na from the tubular fluid if the arriving Na load is relatively small.

26
Q

The Main Integration Point: Explain how the CD is the site where all Na-conserving mechanisms converge.

A

• Low Na delivery to the CD is assured by the action of AII on the TGF and the synergistic actions of AII and catecholamines on proximal tubular Na reabsorption, as well as by aldosterone itself stimulating Na reabsorption in the distal tubule.

27
Q

What is the rate-limiting step in the operation of the RAAS?

A

The rate-limiting step in the operation of the RAAS is release of renin from the granular cells of the afferent arterioles.

28
Q

What mechanisms control this rate-limiting step of RAAS? (Note: we want to increase ECFV)

A
  • a) Reduced blood pressure increases renin secretion, while increased renal perfusion inhibits renin release.
  • b) The afferent arterioles are innervated by sympathetic fibers; sympathetic activation stimulates renin release.
  • These two effects (a and b) are synergistic.
  • c) The granular cells also receive signals from the macula densa that is independent of renal nerve activity. A decrease in NaCl load arriving to the macula densa increases renin release.
  • d) Pressor hormones, AII in particular, provide a negative feedback control for renin production: increased level of pressor hormones inhibits renin release.
  • e) Several hormones like prostaglandins, nitric oxide and ANP play an additional auxiliary role in the regulation of renin secretion.
29
Q

Explain the regulation of aldosterone synthesis.

A
  • AII is the most important regulator
  • ANP plays only a minor role by inhibiting aldosterone production during extreme volume expansion.
  • also regulated by plasma [K]
30
Q

How do sympathetic innveration on the tubules affect Na reabsorption?

A
  • In addition to afferent arterioles, the proximal tubule cells (and to a lesser extent other nephron segments) are also innervated by sympathetic fibers.
  • In the proximal tubule, activation of these fibers acts synergistically with AII to stimulate Na reabsorption.
31
Q

What is ANP? Where is it made? What is BNP? What are their functions?

A
  • ANP promotes natriuresis (Na excretion)
  • This hormone is made in the heart and is released in response to distension of the atria.
  • BNP (brain natriuretic peptide), a peptide with similar structure and activity, is also produced and released by the ventricles.
  • The function of these peptides is to protect the heart from an overload.
32
Q

How do ANP and BNP protect the heart from an overload?

A
  • They reduce cardiac contractility
  • They dilate resistance vessels, venules and large veins, and thereby reduce both preload and afterload.
  • Natriuretic peptides also increase capillary permeability, which allows fluid to seep out from the plasma into the interstitium, thus further relieving the heart.
  • Finally, ANP also promotes renal Na excretion through several mechanisms
33
Q

What are the several mechanisms that ANP uses to promote renal Na excretion?

A
  • It increases GFR and medullary blood flow
  • Inhibits Na reabsorption, particularly in the medullary CDs
  • Inhibits both renin and aldosterone production.
  • inhibiting ADH secretion and antagonizing its action in the CD.
34
Q

What is Pressure Natriuresis? What is its mechanism?

A

• The kidney has an intrinsic capacity to increase the rate of Na as “back-up” system for regulating ECFV.
• With an increase in perfusion pressure, Na reabsorption is inhibited resulting in an exponential increase in Na excretion in spite of a constant GFR (which is autoregulated).
o Pressure diuresis is in part mediated by changes in intrarenal dopamine, NO and prostaglandin levels and by changes in medullary blood flow.

35
Q

Why are the kidneys an ideal site to regulate Red Blood Cell count (through erythropoietin)?

A
  • The kidneys control also regulate ECFV through RBC volume and erythropoietin (Epo).
  • As renal profusion increases, demand for O2 increases, therefore the PaO2 and PvO2 remain constant, unless there are too few or too many blood cells. the kidney an ideal site to monitor changes in arterial pO2 and O2 carrying capacity.
36
Q

What tissue/cell produces Epo? What regulates Epo secretion?

A
  • Epo is produced by interstitial fibroblasts residing between the convolutions of proximal tubules
  • Epo secretion is regulated by the local pO2 in those fibroblasts.
  • This localization allows Epo-secreting cells to integrate arterial pO2 and O2 carrying capacity with changes in ECFV and its derivative, plasma volume.
  • From this information the kidney can decipher total RBC volume.
37
Q

Thought Question: What happens to Epo when there is ECFV contraction with normal total RBC volume (i.e. hemoconcentration)?

A
  • In a state of ECFV contraction with normal total RBC volume (i.e. hemoconcentration), O2 carrying capacity of the blood will increase,
  • BUT so will proximal tubular O2 consumption, because Na reabsorption in the PT is stimulated by AII and catecholamines.
  • Consequently, pO2 in the vicinity of the Epo-secreting cells will remain unaltered.
  • Therefore, RBC levels are able to be monitored independently of blood pressure
38
Q

Thought Question: What happens to Epo when there is ECFV expansion with normal total RBC volume (i.e. hemoconcentration)?

A

• Similarly, in ECFV expansion, the lower O2 carrying capacity of the blood (due to hemodilution) is balanced by the reduced O2 consumption by the PT and thus tissue pO2, and therefore Epo production is unaffected.

39
Q

Thought Question: What happens to Epo in the case of polycythemina (a genuine increase in total RBC volume)? What about in the case of anemia?

A
  • On the other hand, in polycythemia (a genuine increase in total RBC volume) proximal Na reabsorption (and O2 consumption) is normal or low, and thus tissue pO2 becomes elevated, which suppresses Epo release.
  • Conversely, in “true” anemia, tissue pO2 is reduced and more Epo will be secreted.
40
Q

What are symptoms of hypovolemia?

A 
Muscle weakness
Lower BP and Tachycardia
Olinguria
DECREASED Urinary Na
DECREASED  GFR
Increased plasma protein due to protein loss
Polycythemia (increases hematocrit)
decreased skin turgor
Fainting (syncope), lassitude, anorexia, nausea
41
Q

What are the symptoms of hypervolemia?

A 
Increased blood pressure
Orthopnea (shortness of breath)
paroxysmal nocturnal dyspnoea (shortness of breath at night)
Atherosclerosis, aortic dissection (blood flow in layers of smooth muscle)
heart disease and failure
Glomerular damage
Increased protein in urine
Renal failure
vision loss, headache, stroke
Pitting Edema
42
Q

What are the renal effects of sympathetic nerves?

A

Afferent tone increase (GFR increase)
Renin secretion increase
Na reabsorption in proximal tubule increase

43
Q

Angiotensin II and Norepi both affect what renal channel?

A

Na H exchanger in the PT

44
Q

What are the biological RENAL activities of AII?

A 
Na reabsorption in proximal tubule Increase
Renin secretion Increase
Efferent tone INCREASE ALOT
Afferent tone  increase
Medullary flow decrease
Sensitivity of TGF increase
45
Q

What are the biological EXTRARENAL effects of AII?

A 
Aldosterone secretion INCREASE ALOT
Arteriolar tone INCREASE
Thirst increase
Na appetite increase
Sympathetic tone increase
Norepinephrine release increase
Norepinephrine reuptake decrease
Vagal tone decrease
Sensitivity of baroreceptor reflexes decrease
46
Q

What are the factors of increase renin release?

A

Afferent arteriolar pressure decreased
Sympathetic tone {ß-adrenerg.} increased
NaCl load at macula densa decreased
Pressor hormones {especially AII} decreased

47
Q

What are the cellular actions of aldosterone?

A

increases luminal Na channels and basolateral Na/K channels in the DT and CD

48
Q

What blocks Na channels in the CD?

What drugs are examples of these?

A

“K sparing diuretics”
Amiloride
Triamterine

49
Q

Both cortisol and aldosterone cause increase of transcription of luminal Na channels and basolateral Na/K channels. What blocks cortisol’s action? What blocks the blocker? (increases cortisol effect on transcription)

A

11 beta hydroxylsteroid dehydrogenase converts cortisol into a product that does not bind to the transcription factor.
Licorice inhibits 11 B-HSD

50
Q

What are the biological activities of aldosterone?

A

Increases all of the following:
Na reabsorption in DT, CD, sweat glands, colon, and salivary glands
Na sensitivity of taste buds and salt appetite
K excretion
Acid excretion

51
Q

What are the RENAL effects of ANP?

A 
Medullary flow increase
Na reabsorption in IMCD decrease
Afferent tone decrease (GFR increase)
Renin secretion decrease
ADH sensitivity of CD decrease
52
Q

What are the extrarenal effects of ANP?

A 
Cardiac contractility decrease
Venous tone decrease
Capillary permeability increase
Sympathetic tone decrease
Arteriolar tone decrease
Aldosterone secretion decrease
ADH secretion decrease
53
Q

See slides 55 through 57 of ECFV for concept maps

A

Done

54
Q

Dehydration ≠ Volume Depletion
Overhydration ≠ Volume expansion
The size of the extracellular fluid compartment is determined by the AMOUNT of Na in the body.
The amount of Na in the body is determined by the balance of Na intake vs. loss.
The kidneys are the primary regulators of Na balance.
The kidneys regulate not only their own rate of Na excretion but also the rate of Na loss via other routes (GI tract and sweat) as well as the rate of Na intake.
Equivalent changes in Na content and ECFV are assured by osmoregulation.
ECFV, plasma volume and BP tend to change in parallel.
The kidneys regulate both plasma and red cell volume.

A

Done

Physiology Renal Quiz 2 (4 decks)

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