Attributes | Values |
---|
rdf:type
| |
http://linked.open...gbank/description
| - Ramipril is a prodrug belonging to the angiotensin-converting enzyme (ACE) inhibitor class of medications. It is metabolized to ramiprilat in the liver and, to a lesser extent, kidneys. Ramiprilat 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). Ramipril may be used in the treatment of hypertension, congestive heart failure, nephropathy, and to reduce the rate of death, myocardial infarction and stroke in individuals at high risk of cardiovascular events. (en)
|
http://linked.open...y/drugbank/dosage
| |
http://linked.open...generalReferences
| - # Cacciapuoti F, Capasso A, Mirra G, De Nicola A, Minicucci F, Gentile S: Prevention of left ventricular hypertrophy by ACE-inhibitor, ramipril in comparison with calcium-channel antagonist, felodipine. Int J Cardiol. 1998 Jan 31;63(2):175-8. "Pubmed":http://www.ncbi.nlm.nih.gov/pubmed/9510492 # Kleinert S: HOPE for cardiovascular disease prevention with ACE-inhibitor ramipril. Heart Outcomes Prevention Evaluation. Lancet. 1999 Sep 4;354(9181):841. "Pubmed":http://www.ncbi.nlm.nih.gov/pubmed/10485736 (en)
|
http://linked.open...gy/drugbank/group
| |
http://linked.open...drugbank/halfLife
| - Plasma concentrations of ramiprilat decline in a triphasic manner. Initial rapid decline represents distribution into tissues and has a half life of 2-4 hours. The half life of the apparent elimination phase is 9-18 hours and that of the terminal elimination phase is > 50 hours. Two elimination phases occur as a result of ramiprilat's potent binding to ACE and slow dissociation from the enzyme. The half life of ramiprilat after multiple daily doses (MDDs) is dose-dependent, ranging from 13-17 hours with 5-10 mg MDDs to 27-36 hours for 2.5 mg MDDs. (en)
|
http://linked.open...ugbank/indication
| - For the management of mild to severe hypertension. May be used to reduce cardiovascular mortality following myocardial infarction in hemodynamically stable individuals who develop clinical signs of congestive heart failure within a few days following myocardial infarction. To reduce the rate of death, myocardial infarction and stroke in individuals at high risk of cardiovascular events. May be used to slow the progression of renal disease in individuals with hypertension, diabetes mellitus and microalubinuria or overt nephropathy. (en)
|
http://linked.open...bank/manufacturer
| |
sameAs
| |
Title
| |
adms:identifier
| |
http://linked.open...mechanismOfAction
| - 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. Ramiprilat, the principle active metabolite of ramipril, 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. Ramipril 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. (en)
|
http://linked.open...drugbank/packager
| |
http://linked.open...y/drugbank/patent
| |
http://linked.open.../drugbank/synonym
| - Ramipril (en)
- Tritace (en)
- Altace (tn) (en)
- Ramiprilum (en)
- (2S-(1(R*(r*)),2alpha,3abeta,6abeta))-1-(2-((1-(ethoxycarbonyl)-3-phenylpropyl)amino)-1-oxopropyl)octahydrocyclopenta(b)pyrrole-2-carboxylic acid (en)
|
http://linked.open...drugbank/toxicity
| - Symptoms of overdose may include excessive peripheral vasodilation (with marked hypotension and shock), bradycardia, electrolyte disturbances, and renal failure. The most likely adverse reactions are symptoms attributable to its blood-pressure lowing effect. May cause headache, dizziness, asthenia, chest pain, nausea, peripheral edema, somnolence, impotence, rash, arthritis, and dyspnea. LD<sub>50</sub> = 10933 mg/kg (orally in mice). (en)
|
http://linked.open.../drug/hasAHFSCode
| |
http://linked.open...k/foodInteraction
| - High salt intake may attenuate the antihypertensive effect of ramipril. (en)
- Herbs that may attenuate the antihypertensive effect of ramipril include: bayberry, blue cohash, cayenne, ephedra, ginger, ginseng (American), kola and licorice. (en)
- Take without regard to meals. (en)
- Ramipril decreases the excretion of potassium. Salt substitutes containing potassium increase the risk of hyperkalemia. (en)
- Alcohol may increase the vasodilatory effects of ramipril. (en)
|
http://linked.open.../drugbank/mixture
| |
http://linked.open...nk/proteinBinding
| - Protein binding of ramipril is about 73% and that of ramiprilat about 56%. (en)
|
http://linked.open...ynthesisReference
| - Edward Wilson, Martin Beasley, "Stabilized ramipril compositions and methods of making." U.S. Patent US20060134213, issued June 22, 2006. (en)
|
foaf:page
| |
http://linked.open...ugbank/IUPAC-Name
| |
http://linked.open...gy/drugbank/InChI
| |