Angiotensin Converting Enzyme Inhibitors

[kap' toe pril]
[e nal' a pril]

Lisinopril [lye sin'oh pril]
[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) A rapid pressor response,

    • (b) A slow pressor response and

    • (c) 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.

  • 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.

      • Use 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.


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