Univasc

Univasc Uses, Dosage, Side Effects, Food Interaction and all others data.

Univasc is a non-sulfhydryl containing precursor of the active angiotensin-converting enzyme (ACE) inhibitor moexiprilat. It is used to treat high blood pressure (hypertension). It works by relaxing blood vessels, causing them to widen. Lowering high blood pressure helps prevent strokes, heart attacks and kidney problems.

Trade Name Univasc
Availability Prescription only
Generic Moexipril
Moexipril Other Names Moexipril, Moexiprilum
Related Drugs amlodipine, aspirin, lisinopril, metoprolol, losartan, furosemide, carvedilol, hydrochlorothiazide, propranolol, spironolactone
Weight 15mg, 7.5mg,
Type Oral tablet
Formula C27H34N2O7
Weight Average: 498.5681
Monoisotopic: 498.236601452
Protein binding

Moexiprilat is approxomately 50% protein bound.

Groups Approved
Therapeutic Class
Manufacturer
Available Country United States,
Last Updated: September 19, 2023 at 7:00 am
Univasc
Univasc

Uses

Univasc is an angiotensin converting enzyme inhibitor prodrug used to treat hypertension.

For the treatment of hypertension.

Univasc is also used to associated treatment for these conditions: High Blood Pressure (Hypertension)

How Univasc works

Univasc is a prodrug for moexiprilat, which inhibits ACE in humans and animals. The mechanism through which moexiprilat lowers blood pressure is believed to be primarily inhibition of ACE activity. ACE is a peptidyl dipeptidase that catalyzes the conversion of the inactive decapeptide angiotensin I to the vasoconstrictor substance angiotensin II. Angiotensin II is a potent peripheral vasoconstrictor that also stimulates aldosterone secretion by the adrenal cortex and provides negative feedback on renin secretion. ACE is identical to kininase II, an enzyme that degrades bradykinin, an endothelium-dependent vasodilator. Univascat is about 1000 times as potent as moexipril in inhibiting ACE and kininase II. Inhibition of ACE results in decreased angiotensin II formation, leading to decreased vasoconstriction, increased plasma renin activity, and decreased aldosterone secretion. The latter results in diuresis and natriuresis and a small increase in serum potassium concentration (mean increases of about 0.25 mEq/L were seen when moexipril was used alone). Whether increased levels of bradykinin, a potent vasodepressor peptide, play a role in the therapeutic effects of moexipril remains to be elucidated. Although the principal mechanism of moexipril in blood pressure reduction is believed to be through the renin-angiotensin-aldosterone system, ACE inhibitors have some effect on blood pressure even in apparent low-renin hypertension.

Toxicity

Human overdoses of moexipril have not been reported. In case reports of overdoses with other ACE inhibitors, hypotension has been the principal adverse effect noted. Single oral doses of 2 g/kg moexipril were associated with significant lethality in mice. Rats, however, tolerated single oral doses of up to 3 g/kg. Common adverse effects include cough, dizziness, diarrhea, flu syndrome, fatigue, pharyngitis, flushing, rash, and myalgia

Food Interaction

  • Avoid hypertensive herbs (e.g. bayberry, blue cohosh, cayenne, ephedra, and licorice).
  • Avoid potassium-containing products. Potassium products increase the risk of hyperkalemia.
  • Limit salt intake. Salt may attenuate the antihypertensive effect.
  • Take separate from meals. Take 1 hour before meals.

[Moderate] GENERALLY AVOID: Moderate-to-high dietary intake of potassium can cause hyperkalemia in some patients who are using angiotensin converting enzyme (ACE) inhibitors.

In some cases, affected patients were using a potassium-rich salt substitute.

ACE inhibitors can promote hyperkalemia through inhibition of the renin-aldosterone-angiotensin (RAA) system.



MANAGEMENT: It is recommended that patients who are taking ACE inhibitors be advised to avoid moderately high or high potassium dietary intake.

Particular attention should be paid to the potassium content of salt substitutes.

Volume of Distribution

  • 183 L

Elimination Route

Univasc is incompletely absorbed, with bioavailability as moexiprilat of about 13% compared to intravenous (I.V.) moexipril (both measuring the metabolite moexiprilat), and is markedly affected by food, which reduces Cmax and AUC by about 70% and 40%, respectively, after the ingestion of a low-fat breakfast or by 80% and 50%, respectively, after the ingestion of a high-fat breakfast.

Half Life

Univasc elimination half-life is approximately 1 hour. Univascat elimination half-life is 2 to 9 hours.

Clearance

  • 441 mL/min

Elimination Route

Univascat undergoes renal elimination.

Innovators Monograph

You find simplified version here Univasc

*** Taking medicines without doctor's advice can cause long-term problems.
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