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  • 1
    Digitale Medien
    Digitale Medien
    Agmatine recognizes α2-adrenoceptor binding sites but neither activates nor inhibits α2-adrenoceptors (1994)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 351 (1994), S. 10-16 
    Details
    ISSN: 1432-1912
    Schlagwort(e): Key words Agmatine ; α2-Adrenoceptor binding sites ; α2-Adrenoceptors ; Clonidine-displacing substance
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract It has been suggested that agmatine (decarboxylated arginine) is an endogenous clonidine-displacing substance (CDS) which recognizes α2-adrenoceptor and non-adrenoceptor, imidazoline binding sites. We have examined the effect of agmatine at α2-adrenoceptor binding sites and pre- and postjunctional α2-adrenoceptors. Agmatine produced a concentration-dependent inhibition of 1 nmol/l 3H-clonidine binding to both rat (pKi–5.10±0.05) and bovine (pKi–4.77±0.38) cerebral cortex membranes. However, agmatine (0.1–100 μM) failed to activate pre-junctional α2-adrenoceptors regulating transmitter release in the guinea-pig isolated ileum and rat isolated vas deferens, nor did it activate postjunctional α2-adrenoceptors of the porcine isolated palmar lateral vein which mediate contraction or inhibition of forskolin-stimulated cyclic AMP formation. High concentrations of agmatine (10–30-fold the pKi at α2-adrenoceptor binding sites) failed to influence α2-adrenoceptor activation by either clonidine or UK-14304 (5-bromo-6-[2-imidazolin-2-ylamino]-quinoxaline bitartrate) in any of the peripheral preparations examined. Moreover, even in a preparation where an interaction with α2-adrenoceptor binding sites on cell membranes can be demonstrated, the rat cerebral cortex, agmatine failed to inhibit forskolin-stimulated cyclic AMP in the intact tissue or affect the inhibition produced by the selective α2-adrenoceptor agonist UK-14304. Agmatine was also devoid of agonist activity in two preparations, the rat isolated thoracic aorta and the rat isolated gastric fundus, in which CDS has been reported to produce non-adrenoceptor effects. Thus, we have confirmed that agmatine recognizes α2-adrenoceptor binding sites and, therefore, is a CDS. However, since agmatine is devoid of pharmacological activity at either peripheral or central α2-adrenoceptors it can not account for earlier reports suggesting that brain-derived CDS can activate α2-adrenoceptors.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00169058
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  • 2
    Digitale Medien
    Digitale Medien
    Agmatine recognizes α2-adrenoceptor binding sites but neither activates nor inhibits α2-adrenoceptors (1995)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 351 (1995), S. 10-16 
    Details
    ISSN: 1432-1912
    Schlagwort(e): Agmatine ; α2-Adrenoceptor binding sites ; α2-Adrenoceptors ; Clonidine-displacing substance
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract It has been suggested that agmatine (decarboxylated arginine) is an endogenous clonidine-displacing substance (CDS) which recognizes α2-adrenoceptor and non-adrenoceptor, imidazoline binding sites. We have examined the effect of agmatine at α2-adrenoceptor binding sites and pre- and postjunctional α2-adrenoceptors. Agmatine produced a concentration-dependent inhibition of 1 nmol/l 3H-clonidine binding to both rat (pKi–5.10+-0.05) and bovine (pKi–4.77+-0.38) cerebral cortex membranes. However, agmatine (0.1–100 μM) failed to activate pre-junctional α2-adrenoceptors regulating transmitter release in the guinea-pig isolated ileum and rat isolated vas deferens, nor did it activate post-junctional α2-adrenoceptors of the porcine isolated palmar lateral vein which mediate contraction or inhibition of forskolin-stimulated cyclic AMP formation. High concentrations of agmatine (10–30-fold the pKi at α2-adrenoceptor binding sites) failed to influence α2-adrenoceptor activation by either clonidine or UK-14304 (5-bromo-6-[2-imidazolin-2-ylamino]-quinoxaline bitartrate) in any of the peripheral preparations examined. Moreover, even in a preparation where an interaction with α2-adrenoceptor binding sites on cell membranes can be demonstrated, the rat cerebral cortex, agmatine failed to inhibit forskolin-stimulated cyclic AMP in the intact tissue or affect the inhibition produced by the selective α2-adrenoceptor agonist UK-14304. Agmatine was also devoid of agonist activity in two preparations, the rat isolated thoracic aorta and the rat isolated gastric fundus, in which CDS has been reported to produce non-adrenoceptor effects. Thus, we have confirmed that agmatine recognizes α2-adrenoceptor binding sites and, therefore, is a CDS. However, since agmatine is devoid of pharmacological activity at either peripheral or central α2-adrenoceptors it can not account for earlier reports suggesting that brain-derived CDS can activate α2-adrenoceptors.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00169058
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  • 3
    Digitale Medien
    Digitale Medien
    Tumor necrosis factor-alpha induces vitamin D-1-hydroxylase activity in normal human alveolar macrophages (1990)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 142 (1990), S. 652-656 
    Details
    ISSN: 0021-9541
    Schlagwort(e): Life and Medical Sciences ; Cell & Developmental Biology
    Quelle: Wiley InterScience Backfile Collection 1832-2000
    Thema: Biologie , Medizin
    Notizen: The induction of 1-hydroxylase in alveolar macrophages by tumor necrosis factor-alpha (TNF) was examined in view of recent evidence suggesting that local production of 1,25-(OH)2D3 may play a role in the regulation of immune functions. Incubation of pulmonary alveolar macrophages from normal human subjects with recombinant TNF caused a 2- to 10-fold increase in 25-hydroxyvitamin D3-1-hydroxylase activity. The dose-response curve was linear over the range 0.05 - 5.0 IU/ml, and no further increase was seen at higher concentrations. The increase in 1-hydroxylase activity was present after 12 h and reached a maximum after 3 days. The effect of TNF was inhibited in a dose-dependent manner by the presence of 1,25(OH)2D3 (10-10-10-8 M) in the incubation media for 5 days but was unaffected by 10-9 M 1,25(OH)2D3 after 12 h. The enhancement of macrophage 1-hydroxylase activity by TNF was comparable to that induced by gamma interferon (IFN) but the effects of maximal doses of both agents were not additive. The presence of antibody to TNF resulted in a 76% inhibition of TNF-induced 1-hydroxylase but had no significant effect on IFN-induced 1-hydroxylase activity.
    Zusätzliches Material: 3 Ill.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1002/jcp.1041420327
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  • 4
    Digitale Medien
    Digitale Medien
    Effects of ultraviolet irradiation on human skin-derived epidermal cells in vitro (1993)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 157 (1993), S. 119-127 
    Details
    ISSN: 0021-9541
    Schlagwort(e): Life and Medical Sciences ; Cell & Developmental Biology
    Quelle: Wiley InterScience Backfile Collection 1832-2000
    Thema: Biologie , Medizin
    Notizen: The effects of UVA, mixed UVA + B, and solar-simulated irradiation were examined in human keratinocytes and melanocytes cultured in vitro. Irradiation with UVA, UVA + 3, or the solar simulator caused a dose-dependent decrease in keratinocyte cell numbers and thymidine incorporation at 24 hours, with recovery after 48 and 72 hours. Divided dose regimens reduced the inhibitory effect of ultraviolet (UV) irradiation on cell numbers measured 24 hours after the last irradiation. Exposure to both UVA and UVA + B increased formation of cornified envelopes. Similar irradiance doses of UVA 80 minutes (1.12 J/cm2) and UVA + B 40 minutes (1.04 J/cm2) caused 2.4- and 3.3-fold increases in cornified envelope formation, respectively. With solar-simulated irradiation, the cornified envelope formation was increased by 3.5-fold after exposure of 8 minutes (2.6 J/cm2). Irradiation of melanocytes with UVA, UVA + B, or solar-simulated irradiation resulted in a dose-dependent decrease in melanocyte numbers after 24 hours compared with sham-irradiated controls. As a result of UV irradiation, tyrosinase activity of melanocytes measured at 24 hours was stimulated. UVA + B irradiation (1.04 J/cm2) increased tyrosinase activity approximately twofold, while UVA alone (1.1 J/cm2) increased tyrosinase four to sixfold and solar-simulated irradiation (1.3 J/cm2) increased tyrosinase approximately twofold compared to the control cells. Melanin content increased in cells after both UVA and mixed UVA + B irradiation. These results indicate that both UVA and mixed UVA + B irradiation had qualitatively similar effects on the proliferative and functional activity of skin-derived cells but that the type of irradiation and the dosage regimen affect the dose-response relationship. © 1993 Wiley-Liss, Inc.
    Zusätzliches Material: 4 Ill.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1002/jcp.1041570116
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  • 5
    Digitale Medien
    Digitale Medien
    Intervertebral disc degeneration in adult mice with hereditary kyphoscoliosis (1984)
    Hoboken, NJ [u.a.] : Wiley-Blackwell
    Journal of Orthopaedic Research 2 (1984), S. 333-338 
    Details
    ISSN: 0736-0266
    Schlagwort(e): Intervertebral disc ; Mouse mutant ; Kyphoscoliosis ; Life and Medical Sciences
    Quelle: Wiley InterScience Backfile Collection 1832-2000
    Thema: Medizin
    Notizen: Breeding experiments confirmed that a hereditary form of kyphoscoliosis in the BDL strain mouse was due to an autosomal recessive gene (ky). Sagittal sections of whole vertebral columns from adult homozygous recessive mice (ky/ky) were examined histologically. All mice showed varying degrees of degenerative change in one or more intervertebral discs between the fifth cervical and the second thoracic vertebrae. The changes comprised loss of cells, loss of distinction between nucleus pulposus and annulus fibrosus, loss of characteristic ring-like structure in the annulus, and development of wedge-shaped discs. In most animals, degenerative disc substance protruded from the disc space, usually posteriorly, sometimes anteriorly, and occasionally through the vertebral end plate cartilage. Posterior protrusions impinged on the spinal cord.
    Zusätzliches Material: 6 Ill.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1002/jor.1100020405
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