Pharmacology - Renin Angiotensin Aldosterone

Front 1

1. Which cells produce Renin?

2. What is the function of Renin?

3. What is the function of ACE?

4. When is Renin released?

Back 1

1. Juxtaglomerular Cells of the afferent and efferent arterioles

2. Converts Angiotensinogen to AT1

3. Converts AT1 --> AT2

4. When stretch receptors at the JGA sense decreased perfusion
When the Macula Densa receptors detect low Na+
SANS innervates the JGA --> NE --> B1 --> Renin

Front 2

How do the following affect Renin release?

1. Phosphodiesterase Inhibitors, Caffeine, Methylxanthines

2. Angiotensin II

3. ACE inhibitors and ARBs

Back 2

1. Block Na+ recovery --> Mild diuresis
Caffeine blocks ADG release from the Posterior Pituitary

2. Negative Feedback on Renin

3. Block the feedback of ATII on Renin --> Increase Renin

Front 3

1. What receptors do ARBs block?

2. How does this receptor normally become stimulated and what happens after the initial stimulation?

3. What effects does ATII have on the AT2 receptor?

4. Who has the most AT2 receptors?

Back 3

1. AT1 receptors

2. ATII --> Gq --> PLC --> Smooth Muscle Contraction --> Vasoconstriction
Aldosterone synthesis and secretion
ADH secretion
Cardiac Hypertrophy
Vascular Smooth Muscle Cell proliferation
Augmentation of peripheral SANS activity
Renal renin inhibition
Reset Vasomotor center to higher "Normal" BP

3. Vasodilation, Cardiac hypertrophy

4. Fetuses and Neonates

Front 4

1. Functions of Aldosterone

Back 4

1. Na+ absorption at DCT/Cortical Collecting Duct
HypoK+
Alkalosis
Increased Plasma volume
HTN

Front 5

1. What kind of enzyme is ACE?

2. What does it do?

Back 5

1. PDP - Peptidyl Dipeptidase (aka Kinase II)

2. Converts ATI --> ATII
Converts Bradykinin into inactive fragments

Front 6

1. Effects of Bradykinin

2. What are the consequences of ACE Inhibition?

Back 6

1. VAsodilator (Bradykinin II Receptor --> G-protein --> NO --> Decreased arterial resistance and increased venous capacitance)

Proinflammatory (B1 --> Mediates pain, swelling, angioedema
Gq --> PLC --> Bronchoconstrictor --> Induce airway irritability, COUGH, Airway obstruction

2. Captopril Cough (bradykinin)
Hyperk+
Acute Renal Failure
Hypotension (first-dose phenomenon)
Bronchial hyperresponsiveness, ANGIOEDEMA
PAIN

Front 7

How do the following cause Indirect decreases in Renin?

1. Clonidine

2. Beta Blockers

Back 7

1. CNS-active Alpha-2 Agonist --> Decreases SANS --> Decreases NE effect on JGA --> No renin

2. Block NE at the B1 receptor of the JGA --> No renin

Front 8

Renin Antagonist - Aliskerin

1. MOA:

2. Use:

3. What drug is Aliskerin combined with for first line use in HTN?

4. Tox;

Back 8

1. Binds renin

2. HTN
Combo with Diuretics, ACE Inhibitors, ARBs because they increase renin as a side effect

3. Amlodipine (dihydropyridine type Ca2+ channel blocker) --> More effective than either drug alone

4. Pregnancy caution
Mild Diarrhea
Allergy
Cough, Dizzy w/ Hydrochlorothiazide
Dizzy w/ Valsartan or Amlodipine

Front 9

ACE Inhibitors - Captopril, Lisinopril
Prodrugs - Enalapril, Ramipril, Quinapril, Benazepril, Fosinopril
Active Metabolites - Enalaprilat, Ramiprilat

1. Why are ACE Inhibitors used in diabetic patients?

2. MOA:

3. Use:

4. Tox:

5. Contraindications:

Back 9

1. Renal protection

2. Blocks ATI-->ATII

3. HTN, CHF, Diabetes

4. PREGNANCY --> Fetal Renotox
Angiotensin Absence --> Hypotension (first dose phenomenon) --> Acute renal failuer
Aldosterone Absence --> HyperK+
Bradykinin Presence --> Cough, resp irritability, angioedema (swelling throat, lips tongue)
Drug Interactions - K+ sparing duretics or supplements

5. Pregnancy, Renal artery stenosis (ATII constricts the efferent arteriole --> Maintains GFR. Remove ATII --> lose GFR)