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  • 1
    Electronic Resource
    Electronic Resource
    Functional Analysis Of Histamine Receptor Subtypes Involved In Endothelium-Mediated Relaxation Of The Human Uterine Artery (2002)
    Oxford, UK : Blackwell Science Pty
    Clinical and experimental pharmacology and physiology 29 (2002), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. This work was designed to introduce human uterine arteries as a new model for cardiovascular research. Advantages of this model include considerable availability of tissue because of the appearance of uterus myomatosus in post-menopausal women who undergo surgery and the chance to work on dysfunctional and healthy vessels.2. Histamine evoked relaxation of the uterine artery that was prevented by removal of the endothelium or by the presence of NG-nitro-L-arginine.3. Receptor antagonists for histamine H1 (mepyramine) and H2 (ranitidine) receptors increased the EC50 of histamine by 112- and 67-fold, respectively.4. Remarkably, isolated uterine arteries could be stored in incubators for 5 days without any change in contractility to phenylephrine and endothelium-dependent relaxation to acetylcholine and histamine.5. Endothelial cells could be isolated and cultured in high purity, as demonstrated by histochemical staining of factor VIII, low CD45-RO for macrophages and no smooth muscle α-actin. In addition, cultured human uterine artery endothelial cells could be used for single cell Ca2+ measurements.6. In agreement with our findings in the intact vessel, histamine-initiated elevation of the intracellular free Ca2+ concentration was reduced in the presence of mepyramine and ranitidine by 59 and 55%, respectively.7. These data indicate that, in the human uterine artery, H1 and H2 receptors are involved in histamine-induced endothelium-dependent relaxation that is mediated by nitric oxide.8. In addition, this vessel can be stored for possible virus-mediated gene expression for 5 days without any loss of reagibility.9. Finally, endothelial cells can be isolated and cultured from the human uterine artery and maintain their reactivity to histamine in culture.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1440-1681.2002.03704.x
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    ORIGIN AND FUNCTION OF EPOXYEICOSATRIENOIC ACIDS IN VASCULAR ENDOTHELIAL CELLS: MORE THAN JUST ENDOTHELIUM-DERIVED HYPERPOLARIZING FACTOR? (1998)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 25 (1998), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. In addition to their contribution to endothelium-derived hyperpolarization, our understanding of the physiological function of epoxyeicosatrienoic acids (EET) within the vascular wall and the actual enzymes involved in the formation of the EET in endothelial cells is very limited. In the present study, the expression of potential cytochrome P450 (CYP) mono/epoxygenases was assessed in endothelial cells isolated from porcine and bovine aortas as well as in the human umbilical vein-derived cell lines EA.hy926andECV304.2. Expression of CYP2B1, CYP2E1 and CYP3A could be found. The latter were inducible by dexamethasone/cloflbrate for 72 h, a procedure that also enhanced CYP epoxygenase activity in endothelial cells.3. Enzyme induction yielded increases in capacitative Ca2+ entry and membrane hyperpolarization in response to autacoids, such as bradykinin and thapsigargin. Thiopentone sodium, an inhibitor of endothelial CYP mono/epoxygenase(s), diminished autacoid-induced capacitative Ca2+ entry and membrane hyperpolarization, while the effect of EET remained unchanged.4. Epoxyeicosatrienoic acids activated endothelial tyrosine kinase activity in a concentration-dependent manner. Arachidonic acid, at 20-fold higher concentrations, also increased tyrosine kinase activity. Because only the effect of arachidonic acid was inhibited by thiopentone sodium, an inhibitor of CYP mono/epoxygenases, these data suggest that arachidonic acid needs to be converted to the EET in order to stimulate tyrosine kinase.5. All these data provide clear evidence that the CYP epoxygenase-derived arachidonic acid metabolites (EET) not only serve as potential endothelium-derived hyperpolarizing factors but also constitute highly active intracellular messengers with a physiological role including the control of Ca2+ signalling, membrane potential and tyrosine kinase activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1998.tb02162.x
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    Paper (German National Licenses)
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