Drugs online research references
J Cardiovasc Pharmacol. 1987;10 Suppl 2:S80-5.
Ten years of clinical experience with metoprolol.
Vedin A.
Hassle Research Laboratories, Molndal, Sweden.
Metoprolol has been on the market for 10 years; the research, however, started nearly 20 years earlier and clinical research some 17 years ago. Metoprolol has been and is still subject to intensive research, which has resulted in evidence for its cardiovascular protective effects in coronary heart disease, cardiovascular hypertrophy and atherosclerosis. The properties making the beta 1-selective blocker metoprolol a cardioprotective drug and pharmaceutical development improving the qualities of the substance are also discussed in this review.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2444825&dopt=Abstract
Nephron. 1986;43(2):117-22.
Beta adrenergic control of extrarenal potassium disposal. A beta-2 mediated phenomenon.
Bia MJ, Lu D, Tyler K, De Fronzo RA.
Beta adrenergic control of extrarenal potassium disposal was evaluated by examining the effects of physiologic doses of beta adrenergic agonists and antagonists on potassium tolerance in acutely nephrectomized rats. Following an acute intravenous potassium load (0.17 mEq/100 g over 60 min), the plasma potassium concentration rose significantly less in animals concomitantly treated with epinephrine at a dose that raises plasma epinephrine concentration to levels found during surgical stress (maximum plasma K 2.2 vs. 2.9 mEq/1 in controls receiving KCl alone; p less than 0.005). Similar results were observed with the selective beta-2 agonists salbutamol and terbutaline. Conversely, the rise in plasma potassium concentration was significantly greater in rats treated with low-dose propranolol (beta-1 + beta-2 blockade) and with butoxamine (beta-2 blockade) compared to control animals. In contrast, the selective beta-1 blocking agent metoprolol had no effect on potassium tolerance. Alterations in potassium tolerance following the administration of various beta adrenergic agonists and antagonists could not be explained by changes in plasma insulin, renin, or glucose concentration or by differences in the acid-base or hemodynamic status of the animals. The data suggest that beta adrenergic control of extrarenal potassium disposal occurs with physiologic stimulation or blockade of the beta-2 receptor site.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2872603&dopt=Abstract
Diabetes. 1998 Mar;47(3):407-13.
Influence of chronic exposure to high concentrations of D-glucose and long-term beta-blocker treatment on intracellular calcium concentrations of porcine aortic endothelial cells.
Salameh A, Dhein S.
Klinik III fur Innere Medizin, Universitat zu Koln, Cologne, Germany.
Clinical observations indicate that diabetes leads to micro- and macroangiopathy involving endothelial dysfunction. Because recent studies indicate an antiangiopathic effect of celiprolol, but not of metoprolol, in type 1 diabetes, we investigated the direct influence of exposure to high D-glucose concentrations on endothelial cells and the possible effects of both beta-blockers. Nine different chronic treatments were carried out on cultured porcine aortic endothelial cells: 1) 5 mmol/l D-glucose ("normoglycemic" cells), 2) 5 mmol/l D-glucose plus 15 mmol/l L-glucose (osmotic control), 3) 5 mmol/l D-glucose plus 0.5 micromol/l celiprolol, 4) 5 mmol/l D-glucose plus 0.05 micromol/l metoprolol, 5) 5 mmol/l D-glucose plus 0.5 micromol/l celiprolol plus 5 micromol/l propranolol, 6) 20 mmol/l D-glucose ("hyperglycemic" cells), 7) 20 mmol/l D-glucose plus 0.5 micromol/l celiprolol, 8) 20 mmol/l D-glucose plus 0.05 micromol/l metoprolol, and 9) 20 mmol/l D-glucose plus 0.5 micromol/l celiprolol plus 5 micromol/l propranolol. Using the Fura-2 technique, application of either 1 nmol/l bradykinin or 1 micromol/l ATP to the normoglycemic endothelial cells led to a significant increase in intracellular calcium, whereas the hyperglycemic cells showed significantly less reactivity to both agents. Exposure of endothelial cells to L-glucose did not show any difference to normoglycemic controls. Coadministration of 20 mmol/l glucose and celiprolol demonstrated that the alteration of the calcium signal induced by high D-glucose concentrations could be significantly antagonized with celiprolol. In contrast, coincubation with metoprolol failed to normalize the calcium signal. This effect of celiprolol was completely abolished in the presence of propranolol. In normoglycemic cells, none of the beta-blockers influenced the intracellular calcium response to bradykinin or ATP. These results indicate that chronic treatment with high D-glucose concentrations leads to an impairment of calcium signaling, which might be ameliorated by celiprolol.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9519747&dopt=Abstract
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