Drugs online research references
J Hum Hypertens. 1994 Aug;8(8):565-9.
Evidence for stimulation of neutrophil degranulation by selected angiotensin converting enzyme inhibitors in vitro.
Miselis J, Siminiak T, Wysocki H.
Academy of Medicine, Department of Intensive Therapy, Poznan, Poland.
Polymorphonuclear neutrophils (PMN) participate in the development of myocardial injury during ischaemia/reperfusion and granules released by human neutrophils contain proteases capable of activating prorenin in human plasma and can cleave angiotensin II directly from angiotensin I and angiotensinogen. The purpose of the present study was to investigate whether angiotensin converting enzyme (ACE)-inhibitors exert an in vitro effect on PMN degranulation. Isolated neutrophils were incubated with captopril, lisinopril, enalaprilat or ramiprilat and release of lysozyme and myeloperoxidase was measured from unstimulated and opsonised zymosan stimulated cells. All ACE inhibitors increased neutrophil myeloperoxidase release and lysozyme release by both unstimulated and stimulated cells. In the presence of saline unstimulated PMN released 4.48 +/- 0.68% and zymosan-stimulated cells released 7.28 +/- 0.76% of myeloperoxidase content and the enzyme release increased after incubation with captopril (5.55 +/- 0.71 and 8.74 +/- 0.72%), lisinopril (5.43 +/- 0.57 and 9.02 +/- 0.7%), enalaprilat (6.05 +/- 0.67 and 9.20 +/- 0.82%) and ramiprilat (5.82 +/- 0.69 and 9.26 +/- 0.74%), respectively. In the presence of saline unstimulated PMN released 16.71 +/- 1.28% and zymosanstimulated PMN released 34.42 +/- 1.71% of lysozyme content and the release increased after incubation with captopril (21.15 +/- 1.36 and 42.75 +/- 1.95%), lisinopril (23.95 +/- 1.26 and 39.23 +/- 1.94%), enalaprilat (21.34 +/- 1.32 and 41.59 +/- 1.99%) and ramiprilat (20.88 +/- 1.35 and 37.53 +/- 1.95%) by unstimulated PMN, respectively. The ACE-inhibitory effect of these drugs may therefore be decreased by stimulation of PMN degranulation and neutrophil-dependent angiotensin II forming pathway.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7990082&dopt=Abstract
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Sb Lek. 1993;94(2):155-61.
Plasma concentrations of some cardiovascular humoral factors in essential hypertension and their changes during the treatment with converting enzyme inhibitor lisinopril.
Horky K, Jindra A, Peleska J, Jachymova M, Umnerova V, Savlikova J, Jarolim M.
2nd Department of Internal Medicine, 1st Medical Faculty, Charles University, Prague.
Plasma concentration of two main cardiovascular substances - atrial natriuretic factor (ANF) and endothelin - were studied in control subjects (n = 21) under basal conditions and 90 minutes after oral administration of glucose. In hypertensive patients (n = 21) these determinations were repeated after 12 weeks treatment with an angiotensin I-converting enzyme inhibitor lisinopril (Prinivil, Merck Sharp and Dohme). While basal and post-glucose ANF concentrations did not differ in controls and hypertensive patients, a tendency to the higher endothelin levels was found in our group of essential hypertension when compared to normotensive subjects. Glucose loading did not change significantly ANF concentrations in any studied group but significantly lowered plasma endothelin in both controls (from 13 +/- 0.95 to 9.50 +/- 0.95 fmol/ml) and hypertensive patients (from 15.05 +/- 1.23 to 12.15 +/- 1.03 fmol/min). Treatment of hypertensive patients with lisinopril paradoxically increased concentrations of ANF (from 6.43 +/- 2.53 to 11.47 +/- 4.90 fmol/ml) and lowered that of endothelin (from 15.05 +/- 1.23 to 12.17 +/- 1.58 fmol/ml). From our findings we may suggest that the relative predominance of the vasoconstrictor (endothelin) over the vasodilator (ANF) humoral substances might participate in pathogenesis of EH and that the reversal of this disadvantageous ratio after lisinopril (increase of ANF and decrease of endothelin) might contribute to the blood pressure reducing effect of ACEI. The drop in plasma endothelin after glucose remains so far unexplained consequence of glucose loading in both control and hypertensive subjects.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7992008&dopt=Abstract
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J Pharm Biomed Anal. 1999 May;19(6):819-27.
Spectrophotometric and spectrofluorometric methods for the assay of lisinopril in single and multicomponent pharmaceutical dosage forms.
El-Yazbi FA, Abdine HH, Shaalan RA.
Faculty of Pharmacy, Alexandria University, El-Mesallah, Egypt.
Simple and sensitive methods are described for the assay of lisinopril in tablets. The first method (A) is based on the reaction of the drug with chloranil in aqueous solution of pH 9.5 to give yellow colour measured at 346 nm. The second method (B) is based upon the interaction of lisinopril with dichlone resulting in the formation of an intense purple colour measured at 580 nm. The third method (C) depends on the reaction of the drug with acetylacetone and formaldehyde to form a coloured condensation product measured at 356 nm and also has a strong fluorescence at 475 nm (lambda(ex) 410 nm). This method is extended to determine lisinopril in binary mixtures with hydrochlorothiazide. The last method (D) depends on measuring the first and second derivative spectra of lisinopril. Moreover, the derivative method is used as stability-indicating method where lisinopril can be determined in presence of its degradation products. The proposed methods proved to be suitable for a rapid quality control of commercial dosage forms. The results obtained were precise and accurate.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10698547&dopt=Abstract
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