Abstract
ABSTRACTA precise and accurate method for the analysis of antihypertensive drug combination nifedipine and valsartan was developed using the HPTLC method. The stationary phase used was a pre-coated silica gel G60 – F254 aluminium sheet and the mobile phase was acetonitrile: methanol: n-butanol: acetic acid (6:2:2:0.1, v/v/v/v). The detection of spots was carried out densitometrically using a UV detector at 230 nm in the absorbance mode. The Rf values of valsartan and nifedipine were found to be 0.25 and 0.65, respectively. The calibration curve was found to be linear in the range of 120–320 ng/band and 900–2400 ng/band for nifedipine and valsartan, respectively. Forced degradation studies were performed using stress conditions like acid and base hydrolysis, photolytic, thermal and oxidative stress degradation to develop the stability indicating method. The degradation study indicated that nifedipine was susceptible to acid-base hydrolysis, oxidative stress degradation and photolytic degradation, while valsartan was susceptible to acid-base hydrolysis and oxidative stress degradation.
Highlights
Nifedipine (NIF) is chemically dimethyl 1,4-dihydro-2,6dimethyl-4-(nitrophenyl) pyridine-3,5-dicarboxylate
NIF acts by systemic vasodilation via the inhibition of inward flow of calcium ions through L-type calcium channels in cell membranes [3,4,5]
Valsartan is an angiotensin receptor blocker 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
Summary
Nifedipine (NIF) is chemically dimethyl 1,4-dihydro-2,6dimethyl-4-(nitrophenyl) pyridine-3,5-dicarboxylate. The empirical formula of NIF is C17H18N2O6 with a molecular weight of 346.34 g/mol [1,2] (Figure 1). It has an empirical formula C24H29N5O3 and a molecular weight of 435.5 g/mol (Figure 2). Valsartan is an angiotensin receptor blocker 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 AT1mediated vasoconstrictive and aldosterone-secreting effects of angiotensin II and results in a decrease in the vascular resistance and blood pressure. Valsartan is selective for AT1 and has virtually no affinity for AT2 [3,4,6]
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