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Clin Exp Pharmacol Physiol. 1978 Jan-Feb;5(1):17-21.
Comparative studies on the pharmacological actions of antiarrhythmic drugs in isolated rate papillary muscle.

Sugimoto J, Nagata M, Morita M.

1. The effects of ajmaline, cocaine, phenytoin, lignocaine, procainamide, propranolol, quinidine and trimetazidine on the contractility and the refractory period of isolated rat papillary muscles were compared. 2. At the higher concentrations used, all drugs suppressed the contractile tension of the rat papillary muscles. 3. The effects of these drugs on the refractory period were compared at concentrations at which the contractile tension was suppressed by 30% of the control. At this point, lignocaine, procainamide, ajmaline and quinidine prolonged the refractory period more than two-fold while the effects of propranolol and phenytoin were slight, cocaine and trimetazidine had little or no effect.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=639355&dopt=Abstract




Br Med J (Clin Res Ed). 1981 Jun 13;282(6280):1917-9.
Influence of cimetidine on pharmacokinetics of propranolol.

Heagerty AM, Donovan MA, Castleden CM, Pohl JF, Patel L, Hedges A.

Whole-blood propranolol concentrations were estimated for 12 hours after a single 80 mg oral dose was given in six patients taking cimetidine and two weeks after they had stopped the drug. Mean blood propranolol concentrations were higher throughout the sampling period when the patients were taking cimetidine than when they were not, and the difference was statistically significant between one and four hours (p less than 0.05). The mean relative bioavailability of propranolol, measured as the area under the concentration time curve, was significantly higher when the patients were taking cimetidine (p less than 0.025). The mean increase in bioavailability was 136.5 +/- 57.6%, and the results were consistent in each subject. It is concluded from these results that cimetidine reduces the hepatic first-pass extraction of propranolol.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6786672&dopt=Abstract




Neuroendocrinology. 1999 May;69(5):324-30.
Neurotransmitter modulation of glucocorticoid receptor mRNA levels in the rat hippocampus.

Tritos N, Kitraki E, Philippidis H, Stylianopoulou F.

Laboratory of Biology-Biochemistry, Faculty of Nursing, Medical School, University of Athens, Greece.

Glucocorticoids in the hippocampus mediate adaptive responses elicited by stressful stimuli. In this study we investigated glucocorticoid receptor gene expression in the rat hippocampus following acute stress. A significant decrease in glucocorticoid receptor mRNA levels was observed in the hippocampus less than 1 h after the onset of stress. This decrease was inhibited by administering either MK-801, diazepam or propranolol prior to exposure to stress. The effect of diazepam on the stress-induced decrease in hippocampal glucocorticoid receptor mRNA was reversed by Ro-15-1788, suggesting that it is mediated by central benzodiazepine receptors, i.e. GABA-A. These results indicate that NMDA, GABA-A and beta-adrenergic receptors are involved in the mechanism of the stress-induced decrease in glucocorticoid receptor mRNA levels in the rat hippocampus.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10343173&dopt=Abstract













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