Sacubitril, Valsartan
Indications
Sacubitril, Valsartan is used for:
SACUBITRIL
Used in combination with valsartan to reduce the risk of cardiovascular events in patients with chronic heart failure (nyha class ii-iv) and reduced ejection fraction. It is usually administered in conjunction with other heart failure therapies, in place of an ace inhibitor or other arb
VALSARTAN
May be used as a first line agent to treat uncomplicated hypertension, isolated systolic hypertension and left ventricular hypertrophy. May be used as a first line agent to delay progression of diabetic nephropathy. Losartan may be also used as a second line agent in the treatment of congestive heart failure, systolic dysfunction, myocardial infarction and coronary artery disease in those intolerant of ace inhibitors
Used in combination with valsartan to reduce the risk of cardiovascular events in patients with chronic heart failure (nyha class ii-iv) and reduced ejection fraction. It is usually administered in conjunction with other heart failure therapies, in place of an ace inhibitor or other arb
VALSARTAN
May be used as a first line agent to treat uncomplicated hypertension, isolated systolic hypertension and left ventricular hypertrophy. May be used as a first line agent to delay progression of diabetic nephropathy. Losartan may be also used as a second line agent in the treatment of congestive heart failure, systolic dysfunction, myocardial infarction and coronary artery disease in those intolerant of ace inhibitors
Adult Dose
Child Dose
Renal Dose
Administration
Contra Indications
Precautions
Pregnancy-Lactation
Interactions
Adverse Effects
Side effects of Sacubitril, Valsartan :
Mechanism of Action
SACUBITRIL
Sacubitril's active metabolite, lbq657 inhibits neprilysin, a neutral endopeptidase that would typically cleave natiuretic peptides, which includes: atrial natriuretic peptide (anp), brain natriuretic peptide (bnp), and c-type natriuretic peptide (cnp). Anp and bnp are released under atrial and ventricle stress, which activate downstream receptors leading to vasodilation, natriuresis and diuresis. Under normal conditions, neprilysin breaks down other vasodilating peptides and also vasoconstrictors such as angiotensin i and ii, endothelin-1 and peptide amyloid beta-protein. Therefore, the inhibition of neprilysin leads to reduced breakdown and increased concentration of endogenous natriuretic peptides in addition to increased levels of vasoconstricting hormones such as angiotensin ii. (however, when combined with valsartan, would result in blocking of angiotensin ii to its receptor, preventing the vasoconstrictive effects and resulting in a decrease in vascular resistance and blood pressure. ) cardiovascular and renal effects of sacubitril is a result of the increased levels of peptides that are normally degraded by neprilysin
VALSARTAN
Valsartan is an arb that selectively inhibits the binding of angiotensin ii to at1, which is found in many tissues such as vascular smooth muscle and the adrenal glands. This effectively inhibits the at1-mediated vasoconstrictive and aldosterone-secreting effects of angiotensin ii and results in a decrease in vascular resistance and blood pressure. Valsartan is selective for at1 and has virtually no affinity for at2. Inhibition of aldosterone secretion may inhibit sodium and water reabsorption in the kidneys while decreasing potassium excretion. The primary metabolite of valsartan, valeryl 4-hydroxy valsartan, has no pharmacological activity
Sacubitril's active metabolite, lbq657 inhibits neprilysin, a neutral endopeptidase that would typically cleave natiuretic peptides, which includes: atrial natriuretic peptide (anp), brain natriuretic peptide (bnp), and c-type natriuretic peptide (cnp). Anp and bnp are released under atrial and ventricle stress, which activate downstream receptors leading to vasodilation, natriuresis and diuresis. Under normal conditions, neprilysin breaks down other vasodilating peptides and also vasoconstrictors such as angiotensin i and ii, endothelin-1 and peptide amyloid beta-protein. Therefore, the inhibition of neprilysin leads to reduced breakdown and increased concentration of endogenous natriuretic peptides in addition to increased levels of vasoconstricting hormones such as angiotensin ii. (however, when combined with valsartan, would result in blocking of angiotensin ii to its receptor, preventing the vasoconstrictive effects and resulting in a decrease in vascular resistance and blood pressure. ) cardiovascular and renal effects of sacubitril is a result of the increased levels of peptides that are normally degraded by neprilysin
VALSARTAN
Valsartan is an arb that selectively inhibits the binding of angiotensin ii to at1, which is found in many tissues such as vascular smooth muscle and the adrenal glands. This effectively inhibits the at1-mediated vasoconstrictive and aldosterone-secreting effects of angiotensin ii and results in a decrease in vascular resistance and blood pressure. Valsartan is selective for at1 and has virtually no affinity for at2. Inhibition of aldosterone secretion may inhibit sodium and water reabsorption in the kidneys while decreasing potassium excretion. The primary metabolite of valsartan, valeryl 4-hydroxy valsartan, has no pharmacological activity