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Cardiovascular System > Renin-Angiotensin System > Flashcards

Renin-Angiotensin System Flashcards

1
Q

Where in the kidney is high pressure sensed?

A

Juxtaglomerular apparatus, sympathetic nerve endings. Also tubular fluid reaching macula densa.

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2
Q

What secretes renin?

A

Juxtaglomerular apparatus in the wall of the afferent arteriole into lumen of afferent arteriole and renal lymph.

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3
Q

What signals renin secretion increase or decreaes?

A

A renal baroreceptor mechanism in the afferent arteriole that senses changes in renal perfusion pressure Changes in delivery of NaCl (sensed as changes in Cl- concentration) to the macula densa cells of the distal tubule (which lie close to the JG cells and, together, form the “JG apparatus”), Sympathetic nerve stimulation via beta-1 adrenergic receptors Negative feedback by a direct action of Ang II on the JG cells.- AngII up and Renin down.

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4
Q

What is the enzyme activated by renin?

A

Angiotensinogen cleaved into angiotensin I.

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5
Q

What does ACE do?

A

Converts Angiotensin I to Angiotensin II

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6
Q

What factors increase angiotensinogen levels?

A

Hormones- glucocorticoids, estrogens, other sex steroids, pregnancy and thyroid hormone. Inflammatory cytokines -interleukin-1 and tumor necrosis factor. Ang II.

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7
Q

What factors decrease angiotensinogen

A

Adrenal insufficiency Orchiectomy Hypothyroidism. Insulin deficiency.

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8
Q

Where is ACE (angiotensin converting enzyme) located?

A

A membrane-bound exopeptidase and is localized on the plasma membranes of various cell types- vascular endothelial cells, microvillar brush border epithelial cells and neuroepithelial cells.

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9
Q

What other peptides does ACE metabolize?

A

Bradykinin and kallin to inactive metabolites

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10
Q

Role of angiotensin II and aldosterone in the kidney picture

A
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11
Q

What does the renin-angiotensin-aldosterone system regulate?

A

Blood pressure and fluid balance.

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12
Q

What is the main regulator of blood pressure?

A

Angiotensin II through Aldosterone and directly on blood vessels and kidneys.

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13
Q

When is the RAAS activated?

A

Dehydration, thirst, shock, postural changes

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14
Q

RAAS overview picture

A
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15
Q

What are the actions of angiotensin II?

A
  1. Increased sympathetic response
  2. Tubular Na+, Cl- reabsorption and K+ excretion, H2O retention (also from aldosterone)
  3. Adrenal aldosterone secretion
  4. Arteriolar vasoconstriction, increase in BP
  5. ADH secretion (–>H2O absorption)
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16
Q

What is the role of ACE2?

A

Converts Angiotensin II into Angiotensin (1-7) and AngI to Angiotensin (1-9)

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17
Q

What is the role of angiotensin (1-7)?

A

Vasodilation

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18
Q

Flow chart of vasoconstriction and vasodilation of RAAS

A
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19
Q

What are the 2 forms of ectoenzymes of ACE?

A

Somatic and geminal forms

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20
Q

Where is the somatic form of ACE found?

A

Endothelial surface of the lungs and on brush-border membranes of kidney, intestine, placenta, and choroid plexus.

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21
Q

Where is the geminal form of ACE found?

A

Exclusively in testes (crucial role in fertility)

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22
Q

What are the two forms of the somatic form of ACE?

A

Soluble and tissue-bound or membrane-bound form

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23
Q

Where is the soluble somatic form of ACE found?

A

Serum and other body fluids

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24
Q

What is the tissue-bound/membrane bound form of ACE responsible for?

A

Formation of angiotensin II, controls blood pressure and renal function.

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25
Q

Where is ACE2 located?

A

Membrane protein on vascular system, heart and kidney: on heart-endothelium of most intramyocardial vessle, Larger vessels-vascular smooth muscle cells and adventitia , Kidney - endothelium and smooth muscle cells of medium-sized vessels and in proximal tubule epithelial cells.

26
Q

Summary of pressor and depressor arms of RAAS?

A
27
Q

What is the receptor of the pressor arm of the RAAS?

A

AT1 receptor

28
Q

What is the RAAS depressor arm receptor?

A

mas receptor

29
Q

What are the respective effects of ACE and ACE2?

A

Vasoconstriction/dilatino, trophic/anti, fibrotic/anti, sodium reabsorption/natriuresis, inflammation/anti, pro/antithrombotic.

30
Q

What are the predisposing risk factors to cardiovascular and renal damage through the RAAS?

A

Atherosclerosis, diabetes, hypertension, renal failure.

31
Q

How does increase RAAS activity contribute to target organ damage?

A

By BP elevation and overactivation of the system and direct effect of Ang II and aldosterone on blood vessels and cardiac and renal tissues.

32
Q

Potential pathologies of the blood vessels resulting from RAAS?

A

Atherosclerosis, aortic aneurysm, vascular remodeling, endothelial dysfunction

33
Q

What are the contributing factors to accelerated atherosclerosis with the apoE mutation or lacking LDL-receptor?

A

ApoE conserves cholesterol, or LDL can’t absorb. Adding western diet and AngII.

34
Q

What is the mechanism for vessel dysfunction from angiotensin II

A

AngII activates NADPH oxidase which creates reactive oxygen species, dangerous to body. NO scavenges and combines with them to decrease it, which depletes NO and diminishes flexibility of blood vessels-decreased vasodilation.

35
Q

What components of inflammation that cause Angiotensin II to lead to inflammation?

A

AT1 receptor causes cascade leading to dyfunction, apoptosis, injury, monocyte attachment and activation. Direct contraction from AT1 receptors and through depleted NO.

36
Q

What is the mechanism for AngII formation of an aneurysm?

A

Exposure to AngII expands width of aorta and causes inflammatory mechanisms and release of metalloproteinases (MMPs) to form aneurysm. Especially in ApoE deficient mice.

37
Q

Graph of sequential characteristic features of AngII-induced AAAs in hypercholestrolemic mice

A
38
Q

What is the role of the endothelium?

A

Modulates vascular tone and caliber, flow in response to humoral, neural, and mechanical stimuli, Synthesizing and releasing vasoactive substances.

39
Q

What is the normal role of NO?

A

NO produced when endothelium is healthy, potent vasodilator, made from L-Arg.

40
Q

What does cGMP do in the blood vessel?

A

Smooth muscle relaxation.

41
Q

Endothelial cell role in contraction and relaxation of vascular system

A

ATII and Endothelin I cause contraction through AT1 and ETa. NO and PGI2 lead to relaxation through cGMP and cAMP. AngII also depletes NO to decrease relaxation.

42
Q

Cellular mechanisms of Angiotensin II

A
43
Q

How does angiotensin induce plaque rupture?

A
44
Q

What pathological consequence in the heart result from RAAS?

A

Left ventricular hypertrophy
Ventricular remodeling
Electrical remodeling

45
Q

Determinants of left ventricular hypertrophy

A

Circled and underlined are from AngII.

46
Q

What are the consequences of a chronic increase in LV wall stress?

A

Stimulate myocyte hypertrophy
Collagen formation and fibroblasts
Remodelling of the myocardium with a disproportionate increase in fibrous tissue.
Reduce LV compliance
Diastolic dysfunction (at end, d/t decreased compliance, really shown in LV hypertrophy).

47
Q

Non-hemodynamic consequences of AngII

A

Circulating plasma concentrations of Aldosterone and Angiotensin II are related to the extent of LV hypertrophy
Angiotensin II promotes myocyte cell growth (also independent of hemodynamic), and aldosterone increases the collagen content and stimulates the development of myocardial fibrosis from cardiac remodeling.

48
Q

What is ventricular remodeling?

A

Changes in size, shape, and function of the heart after injury to the ventricles

49
Q

How can inhibition of RAAS affect HF?

A

Improves survival and can slow and in some cases even reverse, certain parameters of cardiac remodeling. Decreases infarct size.

50
Q

How can RAAS inhibition affect electrical remodeling?

A

RAAS inhibiton can reduce the incidence of atrial fibrillation after a myocardial infarction and in chronic left ventricular dysfunction.
Angiotensin II may have a role in the mechanism of atrial electrical remodeling, formation of fibrosis and arrhythmias.

51
Q

Angiotensin effects of relevence for arrhythmogenesis

A
  1. Increased wall stress and stretch
  2. Facilitates local NA release and inhibits central vagal activity
  3. Fibrosis
  4. Decreased conduction velocity, disorganized cell-to-cell coupling, increased dispersion of AP durations
  5. Stimulated myocyte growth
  6. Structural vascular changes
52
Q

How does RAAS promote renal injury in patients with renal damage?

A

Intraglomerular hypertension
Glomerular hypertrophy
Albuminuria >500-1000 mg/day

Both diabetic and nondiabetic nephropathy

53
Q

Subclinical pathologies involving angiotensin II

A

Atherosclerosis in carotids without CVA, misshapenness of resistant arteries, shrunken kidneys.

54
Q

What is the effect on decreasing the expression or activity of Angiotenin (1-7)?

A

Susceptibility of the CV system to Ang II pathologies.

55
Q

Comparison of ACE/ACE2 deficient mice

A
56
Q

What are the pharmacological inhibitors of Renin?

A

Beta blockers inhibit renin secretion by stimulation of beta-1 adrenergic receptors. Not direct so weak.

Aliskiren: direct renin inhibitor, prevents angiotensin-angiotensin I.

57
Q

What is the mechanism of ACE inhibitors?

A

Direct vasodilator: blocks bradykinin degradation and conversion of angI into ang II. Not specific to AT1, can also act on other receptors. Also blocks formation of angiotensin(1-7)

58
Q

How do ATR1 Receptor Blockers (ARBs) work?

A

Block AT1 receptor, more specific. Can lead to severe elevation of bradykinins. Not better for survival or morbidity. Complete mechanism and relation to BP decrease unknown.

59
Q

How do patients respond to aldosterone receptor antagonists?

A

Useful treatment.

60
Q

What was the response of HF patients to low doses of aldosterone?

A

Increased survival when added to other meds. Counterintuitive but true (aldosterone usually worsens HF)!

61
Q

What are the beneficial metabolic effects of RAAS blockade?

A

More favorable metabolic profile, increases insulin sensitivity, minimize or prevent diuretic-induced elevations in cholesterol and uric acid levels.

62
Q

Adverse effects of RAAS inhibition

A

Low blood pressure
Failure to increase GFR and/or blood pressure during acute blood pressure reduction (bleeding, dehydration)
Hyperkalemia
ACE-I- angioedema and cough (due to increase in Bradykinin)
Deterioration of renal function in specific patients

Cardiovascular System (28 decks)

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