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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.

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.

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

Imprints


Drug: Enalapril
Strength: 20 Mg
Pill Imprint: W 926
Color: Beige
Shape: Round

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Drug: Enalapril
Strength: 10 Mg
Pill Imprint: W 925
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Strength: 2.5 Mg
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Strength: 2.5 Mg
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Strength: 20 Mg
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Strength: 2.5 Mg
Pill Imprint: VASO 2.5
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Strength: 5 Mg
Pill Imprint: VASO 5
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Strength: 10 Mg
Pill Imprint: VASO 10
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Strength: 20 Mg
Pill Imprint: VASO 20
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Strength: 10 Mg / 25 Mg
Pill Imprint: VASE 10-25
Color: Red
Shape: Elliptical / Oval

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