mid semester Flashcards

1
Q

Discuss the renin-angiotensin aldosterone system and its role in the control of body salt/sodium and water levels.

A

When Arterial blood pressure drops due to the decrease in MAP, the glomerula pressure and GFR will decrease. This drop will activate sympathetic nerves which cause restriction of afferent renal arterioles, in order to decrease NA and water levels excreted in the urine.
By the time the last 10% of filtrate reaches the collecting ducts, hormonal regulation of aldosterone, takes over the reabsorption of Na+.
Aldosterone is the important controller of NA+ reabsorption in the distal tubules/collecting ducts.

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2
Q

Where does aldosterone come from?

A

Aldosterone is secreted form the adrenal glands, which are located on the kidney. Secretion of aldosterone comes from the the outer region of the Kidney cortex called the ZONA GLOMERULOSA.

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3
Q

What type of hormone is aldosterone?

A

Steroid/ mineralocorticoid. This allows the hormone to diffuse through the cell’s plasma membrane without the use of receptors.

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4
Q

Describe the actions of aldosterone on late distal tubules and collecting ducts.

A

Aldosterone exits the peritubular capillaries, and diffuses through the cell membrane.

Inside the cell, it interacts with cytoplasmic mineralocorticoid receptor . This forms a receptor-steroid hormone complex, which diffuses into the cell nucleus. This allows for new protein synthesis.

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5
Q

What proteins are synthesised after the diffusion of the receptor-steroid hormone complex into the nucleus?

A

4 proteins.
These proteins will aid in the absorption of sodium.
Synthesis of new sodium channels and synthesis of Na+/K+ ATPase (pump), which allows sodium to be transported down the gradient.

There is also a synthesis of potassium channels and ATP.

this ultimately leads to increased reabsorption of Na+ in the late distal tubule cells and in the collecting ducts.

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6
Q

Why does it only take 2 hours for the body to get rid of excess H2O, however, takes 6-8 days to get rid of excess Na+?

A

For sodium to be excreted, the cells need to synthesise new proteins and sodium channels are retrieved form the membranes of collecting ducts, to prevent the reabsorption of sodium, and to increase sodium excretion in urine.

However, for water, there a are preformed water channels (aquaporins), and the presence of ADH is going to cause these aquaporins to be inserted into the luminal membrane. No new protein synthesis and thus a RAPID process, in comparison to sodium excretion.

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7
Q

Aldosterone related disease #1:

Addison’s disease

A
Caused by insufficient production of aldosterone by the adrenal glands.
Low blood pressure
salt cravings (hyponatremia= low [Na+] plasma.
Muscle weakness (hyperkalemia= High [K+] plasma)
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8
Q

2: Aldosteronism

A

High blood pressure
Hypernatremia (high [Na] plasma)
Hypokalemia (low [K+] plasma)

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9
Q

What leads to aldosterone secretion?

A

The liver releases a polypeptide ANGIOTENSINOGEN.
this gets converted to Angiotensin I and then to Angiotensin II.
I is converted to II by Angiotensin converting enzyme, secreted from pulmonary and renal epithelial cells.
Angiotensin II then acts on the outer cortex of the adrenal gland to release aldosterone.

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10
Q

List the effects of aldosterone release.

A

it will increase the reabsorption of sodium and secretion of potassium. The overall net effects is you end up with increase water and salt retention.
Increase water and salt retention leads to increased ECF volume, which will bring blood volume back up to norma pressure.

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11
Q

What triggers the Renin-angiotensin aldosterone system?

A

This whole process is triggered when there is a decrease disunion of blood in the kidneys (decreased blood pressure and flow into kidneys), which leads to the secretion of RENIN.
Renin converts the angiotensinogen to the the angiotensin I.

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12
Q

What can be used to treat hypertension/ high blood pressure?

A

ACE inhibitors. Prescribing a drug that prevents Angiotensin II formation.

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13
Q

What is RENIN?

A

Renin converts Angiotensin I to Angiotensin II and is the rate limiting step for Angiotensin II formation.

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14
Q

Where does RENIN come from?

A

Renin is synthesised, stored and released by the granular cells in the juxtaglomerular region of the afferent renal arteriole. Juxtaglomerula cells contain the granules of renin. t These cells are wrapped around the afferent arterioles of the glomerula capillaries.

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15
Q

What stimulates renal secretion

A
  1. Decrease in renal arterial pressure (infrarenal baroreceptors)
  2. Decrease in luminal sodium passing the macula densa.
  3. Increase renal sympathetic nerve activity.
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16
Q

What is the calcium paradox?

A

When there is a decrease In renal arterial pressure, there is a decrease stretch in juxtaglomerular cells. This decrease stretch results in a decrease of calcium release in the cell. However, when increased plasma volume, results in a release of calcium, this decrease renin secretion.

This is referred to as the CALCIUM PARADOX because usually increased cytoplasmic ca++ increases hormone secretion, however this is the opposite in JG cells.

17
Q

Where is the Macula Densa located?

A

In a region of the distal tubules, that faces the JG cells of the afferent renal arteriole.

18
Q

How does increased renal sympathetic nerve activity increase Renin secretion?

A

As JG cells are innervated by sympathetic nerves, when they detect a drop in pressure, there is increased sympathetic nerve innervation of afferent arterioles.

Thus a decrease in body Na+ and blood pressure, results in increased renal sympathetic nerve activity and thus increased activation of Juxtaglomerular Beta receptors and thus renin secretion.

19
Q

Renin-Angiotensin aldosterone system summary

A
  1. one of the 3 renin stimulating factors occur
  2. renin is released
  3. Renin convers angiotensinogen I to angiotensin I
  4. Angiotensin 1 is converted to
    angiotensin II by the angiotensin converting enzyme released by the pulmonary and renal epithelial cells
  5. increase synthesis of angiotensin II, causes increase secretion of ALDOSTERONE.
20
Q

Explain how ANP is secreted and its main effects that lead to natriuresis and lowering of Blood pressure

A

Increase in sodium, leads to increase plasma volume and increased atrial filling. This leads to the secretion of atrial NAP.

21
Q

What is NAP?

A

atrial NATRIURETIC PEPTIDE.

Atrial cells contain molecules called atrial natriuretic peptide.

22
Q

How does ANP lower BP?

acts to decrease pressure by increasing final excretion of sodium.

A

Natriuresis, is the increased release of urinary Na+.
1. acts on collecting ducts to decrease Na+ reabsorption.
2. indirectly, low Na+ reabsorption inhibits renin secretion (and thus aldosterone release)
3. Dilation of afferent and construction of efferent articles. Increase GFR.
less time for excretion , talk later about GFR.

23
Q

Where NAP get its names?

A
  • from ability to increase sodium excretion.