• Benazepril (Lotensin)
• Captopril (Capoten)[kap' toe pril]
• Enalapril (Vasotec)[e nal' a pril]
• Fosinopril (Monopril)

• Lisinopril (Prinvivil, Zestril)[lye sin'oh pril]
• Moexipril (Univasc)
• Quinapril (Accupril)
• Ramipril (Altace) [ram' i pril]

• Angiotensin II, a potent vasoconstrictor, is produced by the action of angiotensin converting enzyme (ACE) on the substrate angiotensin I. Angiotensin II activity produces
  • a rapid pressor response
  • a slow pressor response and
  • vascular and cardiac hypertrophy and remodeling.
• Antihypertensive effects of ACE inhibitors are due to the reduction in the amount of angiotensin II produced.
• ACE inhibitors are efficacious in management of hypertension and have a favorable side effect profile.
• ACE inhibitor are advantageous in management of diabetic patients by reducing the development of diabetic neuropathy and glomerulosclerosis.
• ACE inhibitor are probably the antihypertensive drug of choice in treatment of hypertensive patient who have hypertrophic left ventricles.
  • Hypertensive patients who have ischemic heart disease with impaired left ventricular function also benefit from ACE inhibitor treatment.
• ACE inhibitors reduce the normal aldosterone response to sodium loss (normally aldosterone opposes diuretic-induced sodium loss).
  • Therefore, the use of ACE inhibitors enhance the efficacy of diuretic treatment, allowing the use of lower diuretic dosages and improving control of hypertension.
•  If diuretics are administered at higher dosages in combination with ACE inhibitors significant and undesirable hypotensive reactions can occur with attendant excessive sodium loss.
•  Reduction in aldosterone production by ACE inhibitors also affects potassium levels.
  • The tendency is for potassium retention, which may be serious in patients with renal disease or if the patient is also taking potassium sparing diuretics, nonsteroidal anti-inflammatory agents or potassium supplements.

Captopril (Capoten)

• Overview
  • Orally effective, competitive inhibitor of angiotensin I-converting enzyme (peptidyl dipeptidase) [enzyme converts angiotensin I to angiotensin II (active)]
  • Decreases circulating angiotensin II & aldosterone {angiotensin II stimulates aldosterone secretion by the adrenal cortex}
    •  Compensatory response: increase in angiotensin I & increased renin levels {loss of negative feedback control}
  • Decrease in aldosterone cause slight increase in serum potassium
• Pharmacokinetics:captopril
  • well absorbed; 25%-30% protein bound
  • rapid converting enzyme inhibition (within 15 minutes following oral administration)
  • 50% drug excreted unchanged
  • elimination half-life: two hours -- oxidation, real excretion
• Cardiovascular Effects: captopril (Capoten)
  • Decrease systemic vascular resistance (secondary to a decrease in Na⁺ & water retention)
  • Prominent decrease in renal vascular resistance
  • Reduced systemic blood pressure: no change in heart rate & cardiac output
    • Absence of heart rate change despite reduced blood pressure may suggest alteration baroreceptor sensitivity
  • No orthostatic hypotension (captopril does not interfere with sympathetic nervous system function)
  • captopril may improve vasodilator drug treatment efficacy in management of CHF by blocking vasodilator-induced increases in renin secretion

Adverse Effects

• Angioedema, although rare, may be potentially fatal.

• ACE inhibitiors should not be used during pregnancy.

•  Dry cough.

•  In renovascular hypertension, glomerular filtration pressures are maintained by vasoconstriction of the post-glomerular arterioles, an effect mediated by angiotensin II. Used of ACE inhibitors in patients with renovascular hypertension due to bilateral renal artery stenosis can therefore precipitate a significant reduction in GFR and acute renal failure.

• Initial dose of an ACE inhibitor may precipitate an excessive hypotensive response.