Drugs online research references
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Two new simple and selective assay methods have been presented for the binary mixtures of moexipril hydrochloride (MOEX) and hydrochlorothiazide (HCTZ) in pharmaceutical formulations. The first method depends on second-derivative ultraviolet spectrophotometry with zero-crossing measurements at 215 and 234 nm for MOEX and HCTZ, respectively. The assay was linear over the concentration ranges 1.0-11.0 microg ml(-1) for MOEX and 0.5-9.0 microg ml(-1) for HCTZ. The determination limits for MOEX and HCTZ were found to be 1.0 and 0.5 microg ml(-1), respectively; while the detection limits were 0.2 microg ml(-1) for MOEX and 0.1 microg ml(-1) for HCTZ. The second method was based on isocratic reversed-phase liquid chromatography by using a mobile phase acetonitrile-20 mM phosphate buffer (pH 4.0) (50:50, v/v). Lisinopril was used as an internal standard (IS) and the substances were detected at 212 nm. The linearity range for both drugs was 0.5-12.0 microg ml(-1). The determination and detection limits were found to be 0.100 and 0.010 microg ml(-1) for MOEX and 0.025 and 0.005 microg ml(-1) for HCTZ, respectively. The proposed methods were successfully applied to the determination of these drugs in synthetic mixtures and commercially available tablets with a high percentage recovery, good accuracy and precision.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14550868&dopt=Abstract [PubMed - in process]
int.azg.nl
High sodium intake blunts the efficacy of angiotensin (Ang)-converting enzyme (ACE) inhibition (ACEi), but the underlying mechanism is incompletely characterized. High sodium has been reported to increase vascular expression and vascular activity of ACE. To investigate whether high-dietary sodium-induced effects on vascular conversion of Ang I might be involved in the sodium-induced blunting of the response to ACEi, the authors studied the vasoconstrictor responses to Ang I and Ang II of isolated aortic rings from healthy rats on low dietary sodium (LS: 0.05% NaCl) and high dietary sodium (HS: 2.0% NaCl) after 3 weeks of ACEi (lisinopril 75 mg/L) or vehicle (CON). Blood pressure was similar in LS and HS in CON, but HS blunted the blood pressure response to ACEi. Functional conversion of Ang I was assessed as the difference in dose-response curves to Ang I and Ang II in parallel aortic rings. Sodium intake did not affect the dose-response curves to Ang I and Ang II in CON. In the ACEi groups, a significant difference was present between the curves for Ang I and Ang II on LS (deltaEC50, 6.7 nM; range, 2.2-13 nM; P < 0.01) but not on HS (deltaEC50: 1.3 nM; range, 0.0-4.1 nM, median [interquartile range], NS). Thus, HS blunts the ACEi-induced reduction of functional vascular Ang I conversion compared with LS. Whether the blunted functional vascular conversion is causally related to the blunted blood pressure response remains to be elucidated.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14576507&dopt=Abstract [PubMed - in process]
Pharmacol Res. 2004 Jan;49(1):23-9.
Involvement of nitric oxide and prostaglandin pathways in the cardioprotective actions of bradykinin in rats with experimental myocardial infarction.
Veeravalli KK, Akula A.
Pharmacology Division, Department of Pharmaceutical Sciences, Andhra University, Visakhapatnam 530-003, Andhra Pradesh, India.
Bradykinin is a potent endothelium-dependent vasodilator in the coronary vascular bed. Endothelial mediators released by bradykinin include nitric oxide, prostacyclin and as yet unidentified endothelium-derived hyperpolarising factors. We wished to determine the involvement of nitric oxide and prostaglandin pathways in the cardioprotective actions mediated by bradykinin via the combined inhibition of ACE and aminopeptidase P (APP) in an in vivo rat model of acute ischemia (30 min) and reperfusion (4h). Myocardial infarct size was measured by using the staining agent 2,3,5-triphenyl tetrazolium chloride (TTC). Lipid peroxide levels in serum and in heart tissue were estimated spectrophotometrically. A lead II electrocardiogram was monitored at various intervals throughout the experiment. Infarct size reduction obtained with the combined inhibition of enalapril and apstatin, lisinopril and apstatin was blocked partially but significantly with the prior administration of L-NAME (Nomega-nitro-L-arginine methyl ester) or aspirin, suggesting the involvement of both nitric oxide and prostaglandin pathways in the cardioprotective actions mediated by bradykinin.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14597148&dopt=Abstract [PubMed - in process]
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