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Zestril

Lisinopril (lye-SIH-no-pril, ATC code C09AA is a drug of the angiotensin converting enzyme (ACE) inhibitor class that is primarily used in treatment of hypertension, congestive heart failure and heart attacks.
Historically, lisinopril was the third ACE inhibitor, after captopril and enalapril that was introduced into therapy in early 1990s . Lisinopril has a number of properties that distinguish it from other ACE inhibitors: it is hydrophilic, has long half life and tissue penetration and is not metabolized by the liver. more...

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Pharmacology

Chemistry

Lisinopril is chemically described as (S)-1--L-proline dihydrate. Its empirical formula is C21H31N3O5•2H2O. Lisinopril is the lysine-analog of enalapril. Unlike other ACE inhibitors lisinopril is not a prodrug and tablets contain pharamacologically active substance.

Absorption

After oral dosing peak blood levels are reached within ca. 7 hours. The oral bioavailability is approximately 25% according to measurements of the unchanged drug in urine. The interindividual variability is 6 to 60% within the full dose range of 5 to 80 mg. Emptiness of stomach does obviously not influence the extent of gastrointestinal resorption.

Half life

The halflife of Lisinopril under steady-state conditions is 12.6 hours. The terminal phase shows a prolonged terminal phase, but no cumulation of the drug is seen under normal circumstances.

Metabolism

Lisinopril is not metabolized.

Elimination

Lisinopril is solely excreted in urine in the unchanged form. Elimination of the drug depends on glomerular filtration and tubular excretion. Rate of lisinopril elimination decreases with old age and kindney or heart failure. There is a relation between creatinine and lisinopril clearance. With prolonged therapy dose reduction can be necessary to avoid cumulation.

Lisinopril can be removed from circulation by dialysis.

Mode of action

Lisinopril acts by competitive inhibition of Angiotensin Converting Enzyme (ACE), a key enzyme in the renin-angiotensin system (RAS) which plays a crucial role in controlling of blood pressure. Diminished formation of a potent vasocontrictor - Angiotensin II from Angiotensin I leads to lowering of hypertension. Besides it limits degradation of a vasodilator - bradykinin by ACE. Angiotensin II also increases blood pressure by stimulation the production of aldosterone, which promotes sodium and water retention in the body. So the complete action consists of

  • diminished production of angiotensin II
  • diminished degradation of bradykinin
  • diminished production of aldosterone

Indications

  • hypertension
  • congestive heart failure alone or with diuretics
  • acute myocardial infarction
  • renal and retinal complications of diabetes.

Contraindications and Precautions

As with all angiotensin converting enzyme (ACE) inhibitors

Pregnancy

Category D

When lisinopril therapy in women of child-bearing age is started pregnancy must be excluded and effective contraceptive methods used.

Read more at Wikipedia.org


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Hyperkalemia alert
From Nursing, 11/1/04

ANTIHYPERTENSIVE DRUGS

Patients taking angiotensin-converting enzyme (ACE) inhibitors such as lisinopril (Zestril) or angiotensin-receptor blockers such as irbesartan (Avapro) for hypertension and other cardiovascular conditions should be carefully monitored for potassium overload, according to researchers. About 10% of patients taking ACE inhibitors develop hyperkalemia within a year after the drugs are prescribed. Patients with kidney problems and diabetes are particularly at risk. Signs and symptoms of hyperkalemia include diminished deep tendon reflexes, weakness, palpitations, and arrhythmias.

Patients taking these drugs should avoid taking other drugs and products that impair potassium excretion, including the nonsteroidal antiinflammatory drugs ibuprofen and naproxen, and herbal remedies containing potassium. Teach patients to avoid foods that are high in potassium, such as orange juice, melons, bananas, and salt substitutes.

Source: "Managing Hyperkalemia Caused by Inhibitors of the Renin-Angiotensin-Aldoslerone System," The New England Journal of Medicine, B. Palmer, August 5, 2004.

Copyright Springhouse Corporation Nov 2004
Provided by ProQuest Information and Learning Company. All rights Reserved

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