Renal Part IV Flashcards

1
Q

What do RBF and GFR stand for?

A

Renal blood flow and glomular filtration rate.

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2
Q

What does autoregulation of RBF and GFR mean?

A

RBF and GFR increase only slightly with moderate increases in blood pressure. This facilitates the excretion of excess Na. Autoregulation responds to changes in resistance of the afferent arteriole. In other words, the entry of blood into the kidney regulates GFR and RBF.

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3
Q

What is tubuloglomerular feedback?

A

Increased body fluid volume stimulates homeostatic mechanisms to prevent build up of RBF and GFR. Fluid is controlled by controlling the afferent artery. Too much fluid, the afferent arteriole constricts and fluid speeds up. Not much NaCl is pumped out. The increased NaCl stimulates the macula densa cells. Afferent arteriole constriction decreases the RBF and GFR.

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4
Q

What role does the macula densa play in tubuloglomerular feedback?

A

As flow increases, less time for NaCl to be reabsorbed. Increased tubular levels of NaCl stimulate Na/K/Cl transporters in the macula densa cells. The macula densa cells release adenosine, which constricts the afferent arteriole. The RBF and GFR are restored to normal levels.

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5
Q

What is the myogenic mechanism?

A

The smooth muscle in the afferent arteriole acts as baroreceptors. This elicits a reflexive contraction, which increases resistance to limit blood flow. Decrease in blood pressure relaxes the baroreceptors and smooth muscle. This allows the afferent arteriole to dilate and maintain adequate blood flow.

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6
Q

What Starling forces are involved in regulating the amount of reabsorption?

A

Reabsorption occurs when capillary hydrostatic pressure is lower than that of the tubule. Capillary oncotic pressure is higher than that of the tubule due to a higher concentration of proteins. Fluid flows down the hydrostatic and oncotic gradients from tubule and interstitial fluid into the capillary.

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7
Q

What are starling forces adjusted by?

A

Neuroendicrine mechanism: angiotensin II, aldosterone, sympathetic activity, ADH, natriuretic peptides
Pressure natriuresis

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8
Q

What creates a pressure difference between the arteriole and peritubular and vasa recta capillaries?

A

Efferent arterioles
Afferent arteriole pressure 60 mmHg
Peritubular and vasa recta capillaries 20 mmHg

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9
Q

What fraction of plasma (FF) is filtered?

A

20%.

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10
Q

What is FF (proportion of plasma filtered) determined by?

A

Constriction of the efferent arteriole.

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11
Q

How does altering the efferent arteriole affect reabsorption?

A

Constriction facilitates reabsorption of Na and water. Increasing FF increases capillary proteins and reduces blood flow.
Dilation has the opposite action and facilitates excretion of Na and water.

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12
Q

In neuroendicrine regulation of reabsorption, what is meant by gross regulation of fluid volume?

A

67% of the filtrate in the proximal tube is reabsorbed despite changes in GFR via glomerulotubular balance.

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13
Q

In neuroendicrine regulation of reabsorption, what is meant by fine regulation of fluid volume?

A

Fine regulation of Na levels and extracellular volume is carried out by neuroendocrine control of Na reabsorption in both the proximal and distal portions o the tubule.

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14
Q

What is angiotensin II?

A

Angiotensinogen is formed in the liver and first cleaved by renin to produce angiotensin I. Angiotensin I is then cleaved by ACE to produce angiotensin II.

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15
Q

What is renin?

A

Protease released from the JGA cells due to drop in blood pressure, drop in blood volume, or sympathetic nervous system activity.

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16
Q

How does drop in blood pressure stimulate renin release?

A

Baroreceptors in the afferent arteriole stimulate renin release from the JGA cells.

17
Q

How does drop in blood volume stimulate renin release?

A

Macula densa cells in the distal tubule detect a decrease in tubular Na levels. Macula densa cells then secrete prostaglandins that release renin from the neighboring JGA cells. With low blood flow, more Na is reabsorbed in ascending limb resulting in less Na in JGA to be detected.

18
Q

How does sympathetic nervous system activity stimulate renin release?

A

Increases in response to drop in blood pressure via aortic and carotid baroreceptor reflexes.

19
Q

What is ACE?

A

Angiotensin converting enzyme found on pulmonary and renal endothelial cell surfaces. Converts angiotensin I to angiotensin II.

20
Q

What are the fast, direct actions of angiotensin II?

A

Angiotensin II promotes reabsorption of Na and water in response to drop in blood volume/pressure.
Constricts afferent arteriole to reduce RBF and GFR (less fluid out).
Constricts efferent arteriole, which decreases hydrostatic and increases oncotic pressures in the capillaries (more fluid reabsorbed).
Stimulates proximal tubule cells to reabsorb more Na and water.

21
Q

What are the slow, indirect actions of angiotensin II on the distal tubules and collecting ducts?

A

If the drop in pressure is consistent, angio II stimulates release of aldosterone from the adrenal cortex, ADH from the hypothalamus, and induces thirst from the hypothalamus.

22
Q

What are the 4 neuroendocrine factors that increase reabsorption and decrease excretion in response to a drop in volume/pressure?

A

Angiotensin II, aldosterone, ADH, and sympathetic nervous system

23
Q

What is aldosterone?

A

Steroid that acts on the distal convoluted tubule and collecting ducts.

24
Q

What does aldosterone do?

A

Increases Na reabsorption and K secretion
Up regulates Na/K ATP-ases, Na channels and ATP levels in principal cells
Fine tunes Na levels

25
Q

What is aldosterone secreted by?

A

Adrenal cortex

26
Q

What is aldosterone released in response to?

A
Angiotensin II (due to drop in BP)
High K levels in the blood
27
Q

What are the sympathetic reflexes triggered by?

A

Drops in systemic blood pressure or emotional signals such as fright.

28
Q

What is the mechanism for sympathetic response to a drop in volume/pressure?

A

Aortic and carotid baroreceptors detect drops in arterial pressure and stimulate hypothalamus via the 9th and 10th cranial nerves. Hypothalamus triggers sympathetic activity from the medulla and spinal cord. The brain stem centers activate sympathetic neurons; the preganglionic neurons innervated prevertebral ganglia and the postganglionic neurons innervated arterioles, JGA cells and tubular cells.

29
Q

How does sympathetic activity facilitate water and sodium reabsorption?

A

Stimulates renin release and angiotensin/aldosterone actions
Stimulates sodium reabsorption directly in the proximal tubule cells
Constrict efferent arterioles and vasa recta to promote sodium and water reabsorption via Starling forces.

30
Q

What is RAAS?

A

Renin Angiotensin II Aldosterone Sympathetic

31
Q

What are neuroendocrine factors and processes that decrease reabsorption and increase excretion (in response to an increase in blood volume/pressure)?

A

Decrease RAAS activity
Natriuretic peptides
Pressure natriuresis

32
Q

What are the natriuretic peptides?

A

Atrial natriuretic peptide (ANP)
Brain natriuretic peptide (BNP)
Urodilatin
All 3 peptides are released in response to increased blood volume or pressure and reverse the actions of RAA

33
Q

How do the natriuretic peptides excrete excess Na/water?

A

Increase GFR by dilating the afferent arteriole
Inhibit Na reabsorption by inhibiting Na channels
Inhibit water reabsorption by reducing ADH release
Inhibit secretion of renin and aldosterone

34
Q

What is pressure natriuresis?

A

A physical mechanism that increases urinary excretion if Na and water in response to an increase in blood volume. Plays a major role in long term blood pressure regulation.

35
Q

What is the relationship between pressure natriuresis and NO?

A

Increased shear stress through the vasa recta stimulates release of NO (from arginine) to reduce Na and water reabsorption. NO released from the endothelium vasodilates the vasa recta pericytes, which increases the capillary hydrostatic pressure, which inhibits Na and water reabsorption.

36
Q

What is the relationship between NO and angio II?

A

Angio II and NO a in equilibrium. Both counterbalance the effects in vasoconstriction if the vasa recta.