Manufacturers: King pharmaceuticals inc, Actavis elizabeth llc +12 more
Ramipril is an ACE inhibitor used for the management of hypertension and the reduction of cardiovascular mortality following myocardial infarction in hemodynamically stable patients with clinical signs of congestive heart failure.
Ramipril is an ACE inhibitor used for the management of hypertension and the reduction of cardiovascular mortality following myocardial infarction in hemodynamically stable patients with clinical signs of congestive heart failure.
Ramipril inhibits the RAAS system by binding to and inhibiting ACE thereby preventing the conversion of angiotensin I to angiotensin II. As plasma levels of angiotensin II fall, less activation of the G-protein coupled receptors angiotensin receptor I (ATR) and angiotensin receptor II (ATR) occurs. ATR mediates vasoconstriction, inflammation, fibrosis, and oxidative stress through a variety of signaling pathways. These include G coupling to the inositol triphosphate pathway, activation of phospholipases C, A, and D which contribute to eicosanoid production, activation of Ca-dependent and MAP kinases, G and G, and eventual activation of the Jak/STAT pathway leading to cell growth and production of extracellular matrix components. ATR activation also leads to increased activity of membrane-bound NADH/NADPH oxidase which contributes to production of reactive oxygen species. Decreased activation of this receptor mediates the renoprotective, antihypertensive, and cardioprotective effects of ramipril by reducing inflammation and vasoconstriction. ATR acts in opposition to the effects of ATR by activating phosphotyrosine phosphatases which inhibit MAP kinases, inhibiting Ca channel opening, and stimulating cGMP and nitric oxide production leading to vasodilation. These counteracting effects are shared by the Mas receptor which is activated by Ang(1-7), a subtype of angiotensin produced by plasma esterases from AngI or by ACE2 from AngII produced through a secondary pathway by tonin and cathepsin G. Ang(1-7) also activates ATR although the bulk of its effect is mediated by MasR. ACE is also responsible for the breakdown of bradykinin. The resulting buildup of bradykinin due to ACE inhibition is thought to mediate the characteristic dry-cough as a side effect of ACE inhibitor medications.
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.
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One entry per invention. Patent families filed in the US, EP, WO and CN offices.
