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Home / Drugs / Starting with E / Enalapril

Enalapril is a prodrug that belongs to the angiotensin-converting enzyme (ACE) inhibitor class of medications. It is rapidly metabolized in the liver to enalaprilat following oral administration. Enalaprilat is a potent, competitive inhibitor of ACE, the enzyme responsible for the conversion of angiotensin I (ATI) to angiotensin II (ATII). ATII regulates blood pressure and is a key component of the renin-angiotensin-aldosterone system (RAAS). Enalapril may be used to treat essential or renovascular hypertension and symptomatic congestive heart failure.
Vasotec IV
CategoriesAntihypertensive Agents
Angiotensin-converting Enzyme Inhibitors
ManufacturersApotex inc
Apothecon inc div bristol myers squibb
Ivax pharmaceuticals inc sub teva pharmaceuticals usa
Krka dd novo mesto
Lek pharmaceuticals d d
Mylan pharmaceuticals inc
Ranbaxy laboratories ltd
Sandoz inc
Taro pharmaceutical industries ltd
Teva pharmaceuticals usa inc
Watson laboratories inc
Wockhardt americas inc
Biovail laboratories international srl
Bedford laboratories div ben venue laboratories inc
Hikma farmaceutica (portugal) sa
Hospira inc
Teva parenteral medicines inc
PackagersAdvanced Pharmaceutical Services Inc.
Amerisource Health Services Corp.
Apace Packaging
Apotex Inc.
Apotheca Inc.
A-S Medication Solutions LLC
Baxter International Inc.
Bedford Labs
Ben Venue Laboratories Inc.
Bryant Ranch Prepack
BTA Pharmaceuticals
California Clinical Pharmacy Inc.
Cardinal Health
Comprehensive Consultant Services Inc.
Corepharma LLC
Coupler Enterprises Inc.
Direct Dispensing Inc.
Dispensing Solutions
Diversified Healthcare Services Inc.
Emcure Pharmaceuticals Ltd.
Eon Labs
Heartland Repack Services LLC
Hikma Pharmaceuticals
Hospira Inc.
Ivax Pharmaceuticals
Krka d.d. Novo Mesto
Lake Erie Medical and Surgical Supply
Lek Pharmaceuticals Inc.
Major Pharmaceuticals
Medisca Inc.
Merck & Co.
Merrell Pharmaceuticals Inc.
Murfreesboro Pharmaceutical Nursing Supply
Neuman Distributors Inc.
Nucare Pharmaceuticals Inc.
Ohm Laboratories Inc.
Palmetto Pharmaceuticals Inc.
Par Pharmaceuticals
Patheon Inc.
PD-Rx Pharmaceuticals Inc.
Pharmaceutical Utilization Management Program VA Inc.
Pharmpak Inc.
Physicians Total Care Inc.
Preferred Pharmaceuticals Inc.
Prepackage Specialists
Prepak Systems Inc.
Ranbaxy Laboratories
Rebel Distributors Corp.
Remedy Repack
Sandhills Packaging Inc.
Southwood Pharmaceuticals
Taro Pharmaceuticals USA
Teva Pharmaceutical Industries Ltd.
Tya Pharmaceuticals
UDL Laboratories
Vangard Labs Inc.
Watson Pharmaceuticals
West-Ward Pharmaceuticals
Wockhardt Ltd.
SynonymsEnalapril Maleate
Enalaprila [INN-Spanish]
Enalaprilum [INN-Latin]


For the treatment of essential or renovascular hypertension and symptomatic congestive heart failure. It may be used alone or in combination with thiazide diuretics.


Enalapril is a prodrug that is rapidly metabolized by liver esterases to enalaprilat following oral administration. Enalapril itself has little pharmacologic activity. Enalaprilat lowers blood pressure by antagonizing the effect of the RAAS. The RAAS is a homeostatic mechanism for regulating hemodynamics, water and electrolyte balance. During sympathetic stimulation or when renal blood pressure or blood flow is reduced, renin is released from the granular cells of the juxtaglomerular apparatus in the kidneys. In the blood stream, renin cleaves circulating angiotensinogen to ATI, which is subsequently cleaved to ATII by ACE. ATII increases blood pressure using a number of mechanisms. First, it stimulates the secretion of aldosterone from the adrenal cortex. Aldosterone travels to the distal convoluted tubule (DCT) and collecting tubule of nephrons where it increases sodium and water reabsorption by increasing the number of sodium channels and sodium-potassium ATPases on cell membranes. Second, ATII stimulates the secretion of vasopressin (also known as antidiuretic hormone or ADH) from the posterior pituitary gland. ADH stimulates further water reabsorption from the kidneys via insertion of aquaporin-2 channels on the apical surface of cells of the DCT and collecting tubules. Third, ATII increases blood pressure through direct arterial vasoconstriction. Stimulation of the Type 1 ATII receptor on vascular smooth muscle cells leads to a cascade of events resulting in myocyte contraction and vasoconstriction. In addition to these major effects, ATII induces the thirst response via stimulation of hypothalamic neurons. ACE inhibitors inhibit the rapid conversion of ATI to ATII and antagonize RAAS-induced increases in blood pressure. ACE (also known as kininase II) is also involved in the enzymatic deactivation of bradykinin, a vasodilator. Inhibiting the deactivation of bradykinin increases bradykinin levels and may sustain the effects of enalaprilat by causing increased vasodilation and decreased blood pressure.

mechanism of action

There are two isoforms of ACE: the somatic isoform, which exists as a glycoprotein comprised of a single polypeptide chain of 1277; and the testicular isoform, which has a lower molecular mass and is thought to play a role in sperm maturation and binding of sperm to the oviduct epithelium. Somatic ACE has two functionally active domains, N and C, which arise from tandem gene duplication. Although the two domains have high sequence similarity, they play distinct physiological roles. The C-domain is predominantly involved in blood pressure regulation while the N-domain plays a role in hematopoietic stem cell differentiation and proliferation. ACE inhibitors bind to and inhibit the activity of both domains, but have much greater affinity for and inhibitory activity against the C-domain. Enalaprilat, the principle active metabolite of enalapril, competes with ATI for binding to ACE and inhibits and enzymatic proteolysis of ATI to ATII. Decreasing ATII levels in the body decreases blood pressure by inhibiting the pressor effects of ATII as described in the Pharmacology section above. Enalapril also causes an increase in plasma renin activity likely due to a loss of feedback inhibition mediated by ATII on the release of renin and/or stimulation of reflex mechanisms via baroreceptors. Enalaprilat's affinity for ACE is approximately 200,000 times greater than that of ATI and 300-1000 times greater than that enalapril.


Overdosage may result in marked hypotension and stupor. Most common adverse effects include hypotension, headache, dizziness and fatigue.


~ 60% of absorbed dose is extensively hydrolyzed to enalaprilat, primarily by liver esterases


55-75%, absorption is unaffected by food; enalaprilat (clinically administered IV) is poorly absorbed, 3-12%, due to its high polarity.

half life

< 2 hours for unchanged enalapril in health individuals, may be increased in those with congestive heart failure (3.4 and 5.8 hours for single 5- and 10-mg doses, respectively). The average terminal half life of enalaprilat is 35-38 hours. The effective half life following multiple doses is 11-14 hours.

route of elimination

Excretion of enalapril is primarily renal.

drug interactions

Amiloride: Increased risk of hyperkalemia

Drospirenone: Increased risk of hyperkalemia

Lithium: The ACE inhibitor increases serum levels of lithium

Potassium: Increased risk of hyperkalemia

Rifampin: Rifampin, a strong CYP3A4 inducer, may increase the metabolism of enalapril. Consider alternate therapy or monitor for changes in the therapeutic and adverse effects of enalapril if rifampin is initiated, discontinued or dose changed.

Spironolactone: Increased risk of hyperkalemia

Tizanidine: Tizanidine increases the risk of hypotension with the ACE inhibitor

Tobramycin: Increased risk of nephrotoxicity

Treprostinil: Additive hypotensive effect. Monitor antihypertensive therapy during concomitant use.

Triamterene: Increased risk of hyperkalemia