Drugs online research references
J Cardiovasc Pharmacol. 1990 Mar;15(3):398-407.
Isoproterenol and the genesis of reperfusion-induced arrhythmias in isolated rat heart: adrenoceptor or free radical-mediated mechanisms?
Tosaki A, Woodward B, Yamamoto F, Hearse DJ.
Cardiovascular Research, Rayne Institute, St. Thomas' Hospital, London, U.K.
In the isolated rat heart, reperfusion-induced arrhythmias were exacerbated by isoproterenol (0.01-1.0 microM). The proarrhythmic action of isoproterenol was primarily the result of a beta 1-receptor-mediated tachycardia rather than via a free radical-mediated process, since it was prevented competitively by the beta 1-receptor antagonist metoprolol, but not by the free radical scavengers mannitol, superoxide dismutase, and catalase. If heart rate was maintained by electrical pacing, the protective action of metoprolol against the isoproterenol-induced arrhythmias was lost. At high concentrations (5 and 50 microM), metoprolol alone produced a bradycardia that was probably not related to beta 1 blockade, and this resulted in some nonspecific antiarrhythmic activity. The data provide evidence that, in this model, heart rate during ischaemia is an important determinant of reperfusion-induced arrhythmias, and that free radical formation from the oxidation of high levels of exogenous isoproterenol present at the time of reperfusion does not contribute in a major way to the detrimental action of isoproterenol.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1691363&dopt=Abstract
compuserve.com
Endothelin-1 (ET-1) plays an important role in atherogenesis. The aim of the study reported here was to investigate the effects of the third generation beta-blockers nebivolol and carvedilol on ET-1 liberation, preproendothelin-1 production and on proliferation of human coronary cells. Human coronary endothelial (HEC) and smooth muscle cells (HCSMC) were grown with carvedilol or nebivolol (10(-7)-10(-5) mol/l). Incubation for 1, 2 or 7 days resulted in an 80% concentration- and time-dependent reduction in HCSMC proliferation. beta-blockers such as propranolol or metoprolol did not influence cell proliferation. Nebivolol (10(-7) mol/l) inhibited accelerated HCSMC proliferation in the presence of growth factors such as transforming growth factor-beta1 or platelet-derived growth factor BB. During incubation with nebivolol or carvedilol ET-1 secretion decreased. For nebivolol this is a result of a reduction in preproendothelin-1 mRNA levels. beta-blockers of the third generation that reduce the cell proliferation and ET-1 secretion may represent strategies with great promise for antiproliferative therapy of coronary heart disease.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11078433&dopt=Abstract
Diabetes Res Clin Pract. 1994 Nov;26(1):67-75.
Nicardipine may impair glucose metabolism in hypertensive diabetic patients.
Sasaki H, Naka K, Kishi Y, Ohoshi T, Hagihara T, Matsuo H, Sowa R, Matsumoto G, Sanke T, Nanjo K.
First Department of Medicine, Wakayama University of Medical Science, Japan.
The respective effects of 6 month's administration of beta-blockers (atenolol, metoprolol, carteolol and arotinolol), calcium-channel blockers (nicardipine, diltiazem) and angiotensin converting enzyme inhibitor (enalapril) on hemoglobin A1c (HbA1c) levels were evaluated in hypertensive patients with non-insulin-dependent diabetes mellitus (NIDDM), using a retrospective method. NIDDM patients with stable HbA1c and body weight were selected for this study. The following results were obtained. (1) The administration of nicardipine or beta-blockers significantly elevated HbA1c levels. (2) The administration of diltiazem or enalapril did not have any influence on HbA1c levels. These findings suggest that not only beta-blocker but nicardipine (dihydropyridine type calcium-channel blocker) may cause deterioration in glucose metabolism in NIDDM patients.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7533075&dopt=Abstract
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