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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) Rapid pressor response,

    • (b) 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.