SCT II - Renal Humoral Regulation Flashcards

1
Q

What is RAAS

A

Renin-Angiotensin-Aldosterone-System

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2
Q

How is Angiotensin-II activated?

A

Angiotensinogen released in Liver

Renin (via kidneys) converts Angiotensinogen to Angiotensin-I

ACE (Angiotensin-converting-enzyme via lungs) converts Angiotensin-I to Angiotensin-II

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3
Q

What stimulates Renin production in the kidney?

A
  1. Low kidney perfusion
  2. Low tubular [Na+]
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4
Q

What is the function of Angiotensin-II?

A

Stimulates VASOCONSTRICTION
- Increasing TPR
- Increasing MAP

Stimulates Aldosterone release
Increasing [Na+] + [H2O] reabsorption
- Increases Plasma Volume
- Increases MAP

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5
Q

What is the function of ADH/Vasopressin?

A

V1 Receptors
- Vasoconstriction
- TPR INC
- MAP INC

V2 RECEPTORS
- Water reabsorption
- Blood Volume INC
- MAP INC

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6
Q

How is ANF (ANP) produced?

A

Atrial Natriuretic Factor (Peptide) is produced by the atria if there’s too much blood volume, causing it to stretch

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7
Q

What is the function of ANF (ANP)?

A

Opposite of ADH (Vasopressin)

Increasing diuretics (urinating)
Stimulates VASODILATION
- TPR DEC
- MAP DEC
- Blood Volume DEC

Inhibits Aldosterone
- [Na+] & [H2O] reabsorption inhibited
- Urine amount increased

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8
Q

Name all vasoconstrictor agents

A
  1. Norepi
  2. Epi (Large conc.)
  3. Angiotensin II
  4. ADH (Vasopressin)
  5. Endothelin-1
  6. Neuropeptide Y
  7. TXA 2
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9
Q

Name all vasodilator agents

A
  1. Epi (Small conc.)
  2. Adenosine
  3. VIP
  4. Badykinin
  5. Prostanoids
  6. Histamine
  7. Serotonin (intact endothelium)
  8. Acetylcholine (intact endothelium)
  9. ANF
  10. Substance P
  11. Adrenomedullin
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10
Q

What are the effects of norepi?

A

β-1 Receptors
Positive tropic effects

α-1 Receptors
Arterial Vasoconstriction

α-1 + α-2 Receptors
Venous Vasoconstriction

  • All increase MAP through TPR & CO
  • Reflex Bradycardia intervenes
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11
Q

What is reflex bradycardia?

A

When the MAP increases due to Norepi, the HR decreases to combat too much BP. This happens via the Baroreceptor reflex.

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12
Q

What is the relationship between SP and SV?

A

SP ~ SV

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13
Q

What is the relationship between DP and TPR?

A

DP ~ TPR

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14
Q

What are the effects of Epi at physiologic concentration (low)?

A

β-1 Receptors
Positive tropic effects

β-2 Receptors
Certain vascular vasodilation

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15
Q

what are the effects of Epi at high concentration?

A

Saturate the β receptors and therefore bind to α receptors which overwrite β receptors.

Causing vasoconstriction?

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16
Q

Where is VIP found? What is its function?

A

Vasodilator

Induces smooth muscle relaxation via Gs proteins

Found in:
- Salivary glands
- Pancreas
- GI tract

17
Q

Where is Bradykinin found? What is its function?

A

Vasodilator

  • Increases blood vessel permeability
  • Increases contraction of non-vascular smooth muscle AKA Bronchoconstriction

Brady = slow
Kinin = contraction

18
Q

How do vasoconstricting agents actually vasoconstrict?

A
  1. Agent binds to endothelium
  2. Endothelium cells release Endothelin
  3. Endothelin contracts smooth muscle
19
Q

How do vasodilating agents actually vasodilate?

A
  1. Agent binds to endothelium
  2. Endothelium cells release NO & PGI2 (Prostacyclin)
  3. Two products cause relaxation of smooth muscle
20
Q

What breaks down Bradykinin? And what’s so special about that enzyme?

A

ACE (Angiotensin-Converting-Enzyme)

Converts Angiotensin-I to Angiotensin-II (Active form)