Competitive inhibition of angiotensin converting enzyme leads to decreased angiotensin II production and its effects.

Competitive inhibition of angiotensin converting enzyme leads to decreased angiotensin II production and its effects.

Competitive inhibition of angiotensin converting enzyme leads to decreased angiotensin II production and its effects.

Eff¬ects are broadly similar to ACE inhibitors. The blocking of AT2 receptors reduces the action of angiotensin II.

CVS
- TPR and Afterload is decreased to a greater extent than preload, and this may result in improved CO in heart failure patients.
- HR is usually unchanged and baroreceptor reflexes also
unchanged.

Renal
- the impairment of Ang-II means that the body is less able to respond to a drop in renal perfusion and this may precipitate failure.

Metabolic
– Accumulation of K+ may occur due to decreased aldosterone.

CVS
- TPR and Afterload is decreased to a greater extent than preload, and this may result in improved CO in heart failure patients.
- HR is usually unchanged and baroreceptor reflexes also
unchanged.

Renal
- the impairment of Ang-II means that the body is less able to respond to a drop in renal perfusion and this may precipitate failure.

Metabolic
– Accumulation of K+ may occur due to decreased aldosterone.

CVS
- TPR and Afterload is decreased to a greater extent than preload, and this may result in improved CO in heart failure patients.
- HR is usually unchanged and baroreceptor reflexes also
unchanged.

Renal
- the impairment of Ang-II means that the body is less able to respond to a drop in renal perfusion and this may precipitate failure.

Metabolic
– Accumulation of K+ may occur due to decreased aldosterone.

Notably as ACE is not inhibited, there is not increased levels of bradykinin, hence there is less cough associated with ARBs and possibly
less vasodilation and peripheral oedema attributed to bradykinin levels

PO. rapidly absorbed, BA: 60-70%

PO. absorbed variably. BA: 30%

PO. 50–60% is absorbed. BA: 30%

PO. Well absorbed from the gut but extensive first pass metabolism leads to BA of 25% to 33%,

25%

25%

75%

98%

2 L/kg

1.7 L/kg

0.1 L/kg

0.48 L/kg

oxidised in the liver and converted to sulphides

not metabolised

Hepatic to the active form, ramiprilat

Hepatic (14%) via CYP2C9 and 3A4 to active metabolite, E-3174 (40 times more potent than losartan)

urine both as active metabolites and unchanged

urine unchanged

Urine (60%) and feces (40%) as parent drug & metab

Urine (4% as unchanged drug, 6% as active

2-4 hours

12 hours

triphasic elimination profile of the active metabolite ramiprilat with T1/2 1-2 hrs, 13-17hrs and >50hrs.

1.5-2 hours
E-3174 6-9 hours

A dry cough may occur especially in patients with pre-existing lung disease.
Caution should be exercised in patients on potassium sparing medications. NSAIDs may precipitate renal failure.

A dry cough may occur especially in patients with pre-existing lung disease.
Caution should be exercised in patients on potassium sparing medications. NSAIDs may precipitate renal failure.

A dry cough may occur especially in patients with pre-existing lung disease.
Caution should be exercised in patients on potassium sparing medications. NSAIDs may precipitate renal failure.

Contraindicated like ACE inhibitors in bilateral renal artery stenosis, and
pregnancy. Caution in sodium depleted patients similar to ACE inhibitors

ACE inhibitor

ACE inhibitor

ACE inhibitor

Angiotensin Receptor Blocker

used for management of hypertension, LV dysfunction post-myocardial infarction and in the setting of heart failure. Its use has been shown to decrease progression of heart failure (disease modifying)

used for management of hypertension, LV dysfunction post myocardial infarction and in the setting of heart failure.
Its use has been shown to decrease progression of heart failure (disease modifying).

used for management of hypertension, LV
dysfunction post myocardial infarction and in the setting of heart failure. Its use has been shown to ↓progression of heart failure (disease modifying).

1. essential and renovascular hypertension
2. diabetic nephropathy
3. congestive cardiac failure, and
4. in patients intolerant of angiotensin-converting enzyme inhibitors (ACEIs).

active drug converted to active metabolites. It is a competitive ACE inhibitor

Active drug that is not metabolised and is excreted directly into urine. It is a competitive ACE inhibitor

prodrug requiring hepatic activation to ramiprilat.
Ramiprilat is a competitive ACE inhibitor

substituted imidazole compound which selectively blocks AT2
receptors throughout the body.

Level 3

Level 3

Level 3

Level 3

moderately potent

highly potent

potent

on/dur 6 hours, prolonged action due to metabolite

oral formulation presented as white tablets in dosage ranging from
12.5mg to 50mg

oral formulation presented as white tablets in dosage ranging from 5mg
to 20mg tablets.

oral formulation presented as tablets or capsules in dosage ranging from
1.25mg to 10mg

presented in 50mg tablets.
Combo not available
(available overseas with thiazide)

PO: doses commenced at 6.25mg TDS and uptitrated

PO: doses commenced at 6.25mg TDS and uptitrated

PO: doses commenced at 2.5 mg Daily and uptitrated

PO: doses 50-100mg daily