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Int J Mol Med. 2000 Nov;6(5):591-4.
The influence of angiotensin converting enzyme inhibitors on lipid peroxidation in sera and aorta of rabbits in diet-induced hypercholesterolemia.

Wojakowski W, Gminski J, Siemianowicz K, Goss M, Machalski M.

Department of Experimental and Clinical Biochemistry, Silesian Medical Academy, 40-752 Katowice, Poland.

In hypercholesterolemia increased lipid and lipoprotein peroxidation occurs. The renin-angiotensin system plays an important role in atherogenesis. Angiotensin II induces smooth muscle cells proliferation and stimulates oxidation of LDL particles and foam cell accumulation. Inhibition of ang II production leads to decrease in lipid peroxide production. The aim of this study was to assess the lipid peroxidation expressed as concentration of thiobarbituric acid reactive species (TBARS) in sera and aorta homogenates after administration of two doses of angiotensin-converting enzyme (ACE) inhibitors (captopril, enalapril and quinapril) in diet-induced hypercholesterolemia in rabbits. Sixty-four New Zealand rabbits were used. Animals were fed with standard fodder, special diet (1% cholesterol content) or special diet + tested ACEI. Two doses of ACE inhibitors were used: i), equivalent to applied to humans, ii), dose 10 times higher. The animals were divided into 8 groups: control, standard fodder; B, special diet; C1, C2, special diet + captopril in doses 2.5 and 25 mg/kg/24 h, respectively; E1, E2, special diet + enalapril in doses 0.75 and 7.5 mg/kg/24 h, respectively; Q1 and Q2, special diet + quinapril in doses 0.75 and 7.5 mg/kg per day, respectively. In cholesterol-fed rabbits and in groups receiving lower doses of tested ACE inhibitors, the serum TBARS concentration at 6 months was significantly higher in comparison to the control. The higher doses of enalapril, quinapril and captopril, prevented the cholesterol-induced rise in TBARS concentration. Lower dose of captopril attenuated the rise in TBARS concentration, it was significantly lower in comparison to group B, but higher than in the control group. In animals from groups B, E1, C1, Q1 TBARS concentration in aortae was significantly higher as compared to control group. Both doses of captopril and higher doses of enalapril and quinapril inhibited the rise of lipid peroxides concentration induced by cholesterol-rich diet.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11029530&dopt=Abstract

Toxicol Appl Pharmacol. 2000 Oct 15;168(2):123-30.
Effects of captopril on interleukin-6, leukotriene B(4), and oxidative stress markers in serum and inflammatory exudate of arthritic rats: evidence of antiinflammatory activity.

Agha AM, Mansour M.

Pharmacology Department, Faculty of Pharmacy, Cairo University, Kasr El-Aini Street, Cairo, 11562, Egypt.

We previously demonstrated that captopril (CP) exhibited a high ability to inhibit enzymatically generated leukotrienes, particularly LTB(4), from stimulated intact human neutrophils. This finding together with the immunosuppressive effect of CP have proposed a possible antiinflammatory activity for the drug. Thus, the present study was conducted to investigate the effect of CP on immunologically mediated chronic inflammation; two models were chosen, namely, Freund's adjuvant arthritis and mixed-type hypersensitivity in rat. The effect of CP was assessed on the basis of physical parameter (paw edema) and biochemical markers in blood and inflammatory exudate. CP was given daily during the course of inflammation development. It was administered ip at three doses, viz. 1, 10, and 100 mg/kg. The results claimed that CP succeeded in suppressing edema evolution in hind paws of Freund's arthritic animals, during all phases of the disease. During the chronic phase of inflammation, in either model, CP reduced the elevated serum and exudate (local) LTB(4) and IL-6 levels. The effect on LTB(4) was more pronounced in the exudate and tended to be dose-related. The antiarthritic effect of CP was also accompanied by augmentation of serum level of protein thiols, with reduction or normalization of elevated systemic and/or local levels of lipid peroxide, superoxide dismutase, and glutathione. It could be concluded that long-term treatment with CP confers a good antiinflammatory activity against arthritis in rat, leading to improvement of the oxidative stress induced by the arthritic insult. The reparative effect of the drug could be mediated via reduction of LTB(4) and IL-6. Copyright 2000 Academic Press.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11032767&dopt=Abstract

Scand J Urol Nephrol. 1993;27(3):301-4.
Involvement of the renin angiotensin system in the pathogenesis of postexercise proteinuria.

Cosenzi A, Carraro M, Sacerdote A, Franca G, Piemontesi A, Bocin E, Faccini L, Bellini G.

Institute of Medical Pathology, University of Trieste, Italy.

Proteinuria after strenuous exercise is common in healthy subjects. The pathophysiologic mechanism of postexercise proteinuria (PEP) is not clear, although the phenomenon has long been known and many explanatory theories have been proposed. It is widely recognized that angiotensin II may increase filtration of protein through the glomerular membrane, and that its concentration in plasma increases during exercise. The aim of this study was to evaluate possible involvement of angiotensin II in the pathogenesis of PEP. Of 25 young volunteers who performed maximal aerobic exercise, eight showed PEP. The exercise was repeated after an interval of at least one week, now 90 minutes after administration of captopril (25 mg). Captopril did not affect the achieved work load of the maximal blood pressure and heart rate during the exercise, but PEP was not found. As it was possible to prevent PEP by administering an angiotensin-converting enzyme inhibitor, the study supports the theory that the renin angiotensin system is involved in the pathogenesis of PEP.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8290907&dopt=Abstract

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