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  • 1
    Electronic Resource
    Electronic Resource
    Effect of In Vivo Administration of Naloxone on ATP-ase's Enzyme Systems of Synaptic Plasma Membranes from Rat Cerebral Cortex (2000)
    Springer
    Neurochemical research 25 (2000), S. 867-873 
    Details
    ISSN: 1573-6903
    Keywords: Cerebral cortex ; ATP-ases ; synaptic plasma membranes ; naloxone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Naloxone is a specific competitive antagonist of morphine, acting on opiate receptors, located on neuronal membranes. The effects of in vivo administration of naloxone on energy-consuming non-mitochondrial ATP-ases were studied in two different types of synaptic plasma membranes from rat cerebral cortex, known to contain a high density of opiate receptors. The enzyme activities of Na+, K+-ATP-ase, Ca2+, Mg2+-ATP-ase and Mg2+-ATP-ase and of acetylcholinesterase (AChE) were evaluated on synaptic plasma membranes obtained from control and treated animals with effective dose of naloxone (12μg · kg−1 i.m. 30 minutes). In control (vehicle-treated) animals specific enzyme activities assayed on these two types of synaptic plasma membranes are different, being higher on synaptic plasma membranes of II type than of I type, because the first fraction is more enriched in synaptic plasma membranes. The acute treatment with naloxone produced a significant decrease in Ca2+,Mg2+-ATP-ase activity and an increase in AChE activity, only in synaptic plasma membranes of II type. The decrease of Ca2+,Mg2+-ATP-ase enzymatic activity and the increased AChE activity are related to the interference of the drug on Ca2+ homeostasis in synaptosoplasm, that leads to the activation of calcium-dependent processes, i.e. the extrusion of neurotransmitter. These findings give further evidence that pharmacodynamic characteristics of naloxone are also related to increase [Ca2+] i , interfering with enzyme systems (Ca2+,Mg2+-ATP-ase) and that this drug increases acetylcholine catabolism in synaptic plasma membranes of cerebral cortex.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1007529826905
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  • 2
    Electronic Resource
    Electronic Resource
    Cyclosporin-induced endothelial dysfunction and hypertension: are nitric oxide system abnormality and oxidative stress involved? (2000)
    Springer
    Transplant international 13 (2000), S. S413 
    Details
    ISSN: 1432-2277
    Keywords: Key words ecNOS ; Nitric oxide ; Cyclosporine ; Hypertension ; Superoxide anions
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Hypertension is a major side effect of cyclosporin (CsA). While the mechanism(s) responsible are unclear, CsA-induced endothelial dysfunction and CsA-induced hypertension have been attributed to the CsA effect on the endothelial-derived factors controlling vasomotor tone. Endothelial nitric oxide (NO) is crucial in the maintenance of a state of basal vasodilation, and recent studies have suggested an NO-mediated counterregulatory mechanism protective from CsA-induced vasoconstriction. Our study evaluates endothelial nitric oxide synthase (ecNOS) gene status (PCR analysis) and plasma levels of NO metabolites (ELISA) in kidney and heart transplant patients under chronic CsA treatment with CsA-induced hypertension. Since CsA increases superoxide production, which metabolises NO, plasma hydroperoxides from cholesterol esters and from triglycerides and peroxynitrite were also evaluated (HPLC) as an index of the presence of superoxides and of “oxidative stress”. Quantification of monocyte ecNOS mRNA and NO metabolites plasma levels from patients and controls (C) demonstrated NO system upregulation in patients notwithstanding the hypertension. The mean ecNOS to β-actin ratio was 1.80 ± 0.85 in patients vs 0.40 ± 0.09 in C (P 〈 0.04). NO metabolites were 34.03 ± 14.32 μM in patients vs 11.53 ± 5.64 μM in C (P 〈 0.001). Hydroperoxides from cholesterol esters and from triglycerides were also increased in patients, 3.4 ± 1.4 vs 1.3 ± 0.6 integrated area units (i. a. u.), P 〈 0.007 and 10.6 ± 6.4 vs 1.3 ± 0.8 i. a. u., P 〈 0.008, respectively, as well as the peroxynitrite plasma level, 0.32 ± 0.11 μM/l vs undetectable in C. This study confirms a CsA-induced NO system upregulation in transplanted patients. However, the NO-mediated counterregulatory system to CsA-induced vasoconstriction, present in normals, could be canceled in patients by CsA-induced superoxide (O2 –) and free radical production which, by increasing NO metabolism, could contribute to CsA-induced vasoconstriction and hypertension and predispose to atherosclerosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001470050374
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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