Drugs online research references
Cell Biol Int. 1998;22(1):13-20.
Modulation of interferon gamma induced increases in cathepsin B in THP-1 cells by adrenergic agonists and antagonists.
Li Q, Bever CT Jr.
Departments of Neurology and Pharmacology and Experimental Therapeutics, Baltimore Veterans Affairs Medical Center, Baltimore, Maryland, 21201, USA.
In order to investigate the possible modulation of macrophage function by the autonomic nervous system, the effect of adrenergic agonists and antagonists on interferon (IFN)-gamma-induced increases in cathepsin B (CB) in a macrophage-like cell line was studied. It has been shown previously that IFN-gamma induces increased CB activity in phorbol myristate acetate (PMA)-primed THP-1 cells. Isoproterenol (ISO) (10 micrometers), a mixed beta-receptor agonist, increased the induction of CB activity in the cells but norepinephrine (10 micrometers) and epinephrine (10 micrometers), the alpha and beta receptor agonists, had little effect. The addition of the mixed alpha-receptor antagonist phentolamine (10 micrometers) had no effect on ISO induced increases but the mixed beta-receptor antagonist propranolol (10 micrometers) and the selective beta1-receptor antagonist atenolol produced significant inhibition. These results suggest that the activation of beta-receptors could be involved in the induction of CB activity in macrophages and provide a possible mechanism for the regulation of macrophage effector function by the autonomic nervous system. Dibutyryl cAMP (1 mm) alone also induced increases in CB in THP-1 cells, and H-89 or HA1004 abrogated the effect of dibutyryl cAMP, suggesting that the effect of ISO on CB could be through the elevation of cAMP and the activation of cAMP-dependent protein kinases. Copyright 1998 Academic Press.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9828078&dopt=Abstract
Eur J Pharmacol. 1981 May 8;71(2-3):223-32.
Effects of right stellate ganglion stimulation on regional myocardial blood flow and ischemic injury in dogs.
Tato F, Berdeaux A, Vilaine JP, Giudicelli JF.
The effects of right stellate ganglion stimulation (RSGS) on regional myocardial blood flow (RMBF) and epicardial ST-segment elevation were investigated in the normal and ischemic myocardium of anesthetized dogs. In the non-ischemic areas and despite the augmentation of cardiac work resulting from the increase in heart rate and in myocardial contractile force, RSGS induced no significant changes in RMBF or in the endo/epi ratio. However, after suppression by atenolol of its chronotropic and inotropic effects, RSGS significantly increased the calculated coronary resistance and reduced RMBF, and combined atenolol + phenoxybenzamine treatments abolished these effects. In the ischemic areas, RSGS had no effect on RMBF, endo/epi and I/NI ratios but increased ST-segment elevation, an effect abolished by atenolol. We conclude that (1) during RSGS, alpha-adrenoreceptor-mediated coronary vasoconstriction contributes to oppose beta 1-myocardial stimulation effects on RMBF and endo/epi ratio, (2) further elevation of ST-segment by RSGS is due to enhancement of oxygen requirements by beta 1-adrenoreceptor stimulation.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7250188&dopt=Abstract
Biochem Pharmacol. 1982 Jul 1;31(13):2263-6.
Inhibition of gastrointestinal mucosal glycoprotein synthesis by the beta-adrenergic blocking drug, practolol.
Okine LK, Ioannides C, Parke DV.
The effect of administration of practolol and other beta-blocking agents on gastrointestinal mucosal glycoprotein synthesis was studied in the rat. Practolol, at a dose of 50 mg/kg, inhibited the incorporation of N-acetylglycosamine into gastric mucosal glycoproteins, while acebutolol, atenolol, pronethalol and propranolol had no inhibitory effect, even at a dose of 200 mg/kg. In addition, practolol inhibited the incorporation of N-acetylneuraminic acid, D-fucose and L-serine into gastric mucosal glycoproteins, while the other beta-blocking agents had no effect. Administration of practolol caused no significant change in the rate of incorporation of glycoprotein precursors into intestinal mucosal glycoproteins. These results indicate that of the beta-blocking drugs studied, inhibition of glycoprotein synthesis is associated only with practolol and is independent of its beta-blocking effect.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6127083&dopt=Abstract
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