RAAS system Flashcards

1
Q

What is Renin?

A

An enzyme released by the JGA. which results in the

formation of angiotensin II.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the Juxtaglomerular apparatus (J GA)?

A

The combination of the tubular cells of the macula densa, granular afferent arteriolar cells that secrete renin, and extraglomerular mesangial cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the Macula densa?

A

A patch of columnar tubular epithelial cells
that forms part of the JGA and may sense tubular ion
concentration. It is situated at the junction of the thick
ascending limb of the loop of Henle and the early distal
tubule.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

The Systemic Blood pressure can vary from 80-180 mm Hg systolic? What is a healthy reference range?

A
  • 120 mm Hg is reference
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What does RAAS stand for?

A

Renin-Angiotensin-Aldosterone System.

RAAS is an important hormone axis effecting the kidney.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What can activate the RAAS system?

A

The system can be activated when there is a:

  • loss of blood volumeor a drop inblood pressure(such as inhemorrhageordehydration). This loss of pressure is interpreted bybaroreceptorsin thecarotid sinus.
  • A decrease in the filtrate NaCl concentration and/or decreased filtrate flow rate will stimulate themacula densato signal thejuxtaglomerular cellsto release renin.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the four stages of RAAS system action?

A
  1. If perfusion at juxtaglomerular apparatusin the kidney’smacula densadecreases, the juxtaglomerular cells (granular cells, modified pericytes in the glomerular capillary) release theenzymerenin.
  2. Renin cleaves a decapeptide from a plasmaα-2-globulincalledangiotensinogen. The 10 amino acid long peptide is known asangiotensin I.
  3. Angiotensin I is then converted toangiotensin IIbyangiotensin-converting enzyme(ACE), found in lung cells and endothelial cells.
  4. Angiotensin II is the major bioactive product of the renin-angiotensin system, binding to receptors onintraglomerular mesangial cells, causing these cells to contract along with systemic blood vessels. Angiotensin II is a potent vasoconstrictor, 40X more potent than epinephrine. Angiotensin II also acts on theadrenal cortexculminating in the release ofaldosteronefrom thezona glomerulosa. Angiotensin II acts as anendocrine,autocrine/paracrine, andintracrinehormone.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What does aldosterone do?

A

Aldosterone, is a steroid hormone produced by the zona glomerulosa of the adrenal cortex in the adrenal gland. It is essential for sodium conservation in the kidney, salivary glands, sweat glands and colon. It plays a central role in the regulation of the plasma sodium (Na+), the extracellular potassium (K+) and arterial blood pressure.
It does so mainly by acting on the mineralocorticoid receptors in the distal tubules and collecting ducts of the nephron.
It influences the reabsorption of sodium and excretion of potassium (from and into the tubular fluids, respectively) of the kidney, thereby indirectly influencing water retention or loss, blood pressure and blood volume.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How does Myogenic feedback work during High BP?

A

HIGH BP —»increased RenaI BIood FIow —»stretches Vascular Smooth Muscle in AFFERENT arteriole—»leads to automatic constriction of afferent =reduces flow to glomerulus = - GFR to minimise damage to renal tissue during high BP.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How does the Myogenic feedback work during Low BP?

A

Low BP -»reduced RBF —»> relaxes Vascular Smooth Msucle in AFFERENT arteriole —»> leads to automatic vasodilatation of afferent = increased flow to glomerulus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the extrinsic mechanisms that kick in when low BP happens?

A

— Extrinsic mechanisms kick in
. Sympathetic Nervous System (vasoconstriction)
. Angiotensin II
. Endothelin to some extent (vasoconstriction)
. Prostaglandins (vasodilate afferent)
. Nitric Oxide (vasodilate afferent)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

The JGA releases renin in response to a drop in:

A
  • afferent arteriolar pressure.
  • a fall in tubular flow rate,
  • or a fall in tubular sodium and chloride concentration at the macula densa
  • Other stimuli include sympathetic nerve stimulation of beta 1-adrenergic receptors.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

ReniN promotes production of Angiotensin II which acts via AT1 (type 1 angiotensin II receptors) to vasoconstrict afferent and efferent arterioles. What is the dominant effect of this?

A

Dominant effect is on efferent arteriolar constriction. so the GFR is increased during low BP.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What does the RAAS enable after a meal?

A

The RAAS enables variable salt intake, whilst
maintaining ECF volume and thus arterial pressure
i.e. 50-fold increase in salt intake —only moves pressure by 5-6mmHg. Without the RAAS, pressure may go up 50-6OmmHg!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Angiotensin II also induces ……………. in aid of the rapid response of the RAAS to restore Na content in body and thus blood volume/BP.

A
Insertion of Na channels in :
*renal tubules via AT1
*In the Proximal tubule
 *In the Thick ascending limb
 *In the Collecting duct
—  via Epithelial Na channel (ENaC)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What do ACE inhibitors do?

A
  • ACE inhibitors inhibit angiotensen II production.
  • They reduce intraglomerular pressure by dilating efferent arterioles more than afferent arterioles. This reduces proteinuria and glomeruloscierosis.

(Complications include hyperkalemia caused by reduced aldosterone production)

17
Q

Inhibition of angiotensin II production by ACE inhibitors

results in:

A

— Lack of vasoconstriction.
— Reduced aldosterone production = decreased renal salt and water
retention = prevent or reduce oedema
— Inhibit hypertrophy of myocardium and vascular smooth muscle
— Decreased water intake.
— Decreased sympathetic activation.
— Decreased vasopressin release.

18
Q

ACE inhibitors (and angiotensin II receptor blockers) are the only vasodilators that directly counteract the effects of the RAA system. Therefore what condition might they play a key role in assisting during it’s treatment with diuretic therapy?

A

Important role of ACE inhibition is to counteract
deleterious RAA system activation associated with diuretic therapy used in patients with congestive heart failure so BP can remain lower and the RAAS is unable to counteract the diuretic therapy.

19
Q

What factors stimulate the RAAs?

A
  • Increased sympathetic activity via renal nerves
  • Increased circulating catecholamines
  • Prostaglandins
20
Q

What factors inhibit the RAAs?

A
  • Increased Na and cr reabsorption across macula densa
  • Increased afferent arteriolar pressure
  • Angiotensin II blockers
  • Vasopressin