Drugs online research references
Arch Biochem Biophys. 1983 Aug;225(1):196-202.
Adrenergic regulation of glycogenolysis in isolated guinea-pig hepatocytes: evidence that beta 2-receptors mediate catecholamine stimulation of glycogenolysis.
Arinze IJ, Kawai Y.
Glycogenolysis in hepatocytes isolated from fed guinea pigs was much more enhanced by the beta-agonist, isoproterenol, than by equimolar concentrations of the alpha-agonists, phenylephrine and norepinephrine. The stimulatory effects of catecholamines occurred with the following order of potency: isoproterenol greater than epinephrine greater than norepinephrine. This order of potency is characteristic of beta 2-adrenergic receptors. That beta 2-receptors are responsible for mediating catecholamine stimulation of glycogenolysis in guinea-pig hepatocytes was further deduced from the inhibition of agonist-stimulated glycogenolysis by beta-receptor sub-type-selective antagonists. Thus, IPS 339, a beta-antagonist which has higher affinity at beta 2-sites than at beta 1-sites, was three orders of magnitude more potent in inhibiting isoproterenol-stimulated glycogenolysis than either atenolol or practolol, both of which are beta 1-selective antagonists. The beta 2-agonists zinterol and procaterol also stimulated glycogenolysis in hepatocytes and their effects were inhibited by propranolol and IPS 339, but not by practolol. Furthermore, activation of phosphorylase in these hepatocytes by isoproterenol, epinephrine, and norepinephrine also occurred with the potency order expected for beta 2-receptors. These results are in sharp contrast to those obtained with rat hepatocytes and emphasize that species differences occur in the regulation of hepatic glycogenolysis by catecholamines.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6311101&dopt=Abstract
J Anal Toxicol. 1990 Mar-Apr;14(2):132-6.
Use of cyclic boronates for GC/MS screening and quantitation of beta-adrenergic blockers and some bronchodilators.
Zamecnik J.
Health and Welfare Canada, Bureau of Drug Research, Ottawa, Ontario.
Gas chromatographic and mass spectrometric properties of cyclic methyl and n-butyl boronates of 13 beta blockers and bronchodilators were investigated for potential use in screening and quantitation in biological materials of interest. The tested compounds included acebutolol, atenolol, labetalol, levobunolol, metoprolol, nadolol, oxprenolol, pindolol, propranolol, sotalol, albuterol, and isoproterenol. The cyclic methyl boronates were superior in gas chromatographic properties to the corresponding n-butylboronates of these compounds. Higher weights of fragments obtained with n-butyl boronation may be advantageous for analyses of complex biological matrices. Mass spectra and retention times relative to SKF-525A are provided.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1969974&dopt=Abstract
J Clin Endocrinol Metab. 1990 Jan;70(1):56-61.
Atenolol enhances nocturnal growth hormone (GH) release in GH-deficient children during long term GH-releasing hormone therapy.
Martha PM Jr, Blizzard RM, Thorner MO, Rogol AD.
Department of Pediatrics, University of Virginia Health Sciences Center, Charlottesville 22908.
The effect of the selective beta 1-adrenergic blocking agent atenolol (50 or 100 mg, orally) on spontaneous and GH-releasing hormone (GHRH)-stimulated GH release was evaluated in six GH-deficient children during long term therapy with GHRH. Nocturnal GH concentrations were determined every 20 min for 12 h under the following four conditions: 1) control, 2) atenolol administration only, 3) sc GHRH administration only, and 4) combined GHRH and atenolol administration. The mean 12-h nocturnal GH concentrations after administration of atenolol alone [2.4 +/- 0.6 microgram/L (mean +/- SEM)] or GHRH alone (2.7 +/- 1.0 micrograms/L) were indistinguishable from baseline values (2.0 +/- 0.5 microgram/L; P greater than 0.05). In contrast, the addition of atenolol to ongoing GHRH therapy caused a clear augmentation of 12-h overnight GH release compared to that during all other study periods (5.0 +/- 1.3 micrograms/L; P less than 0.05). In a subset of three subjects for whom GH pulse characteristics were determined, the primary mode of the enhanced GH release was through an increase in the amplitude of serum GH pulses. These results are consistent with the hypothesis that beta-adrenergic blocking compounds enhance the responsivity of the pituitary gland to agents that permit GH release by inhibiting hypothalamic somatostatin secretion or action. They suggest that atenolol may have potential as an adjunctive therapy in some children with abnormalities of GH secretion when GHRH is the primary therapeutic agent.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2104629&dopt=Abstract
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