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Ennio Ongini - One of the best experts on this subject based on the ideXlab platform.

Jon D. Levine - One of the best experts on this subject based on the ideXlab platform.

  • modulation of bradykinin induced plasma extravasation in the rat knee joint by sympathetic co transmitters
    Neuroscience, 1993
    Co-Authors: Paul Green, J Luo, Philip H Heller, Jon D. Levine
    Abstract:

    We describe the contribution of various sympathetic post-ganglionic neuron mediators to bradykinin-induced plasma extravasation in the knee joint of the rat. Co-perfusion of the sympathetic post-ganglionic neuron mediators, norepinephrine or neuropeptide Y with bradykinin resulted in diminished plasma extravasation. In contrast, the putative sympathetic post-ganglionic neuron mediators of bradykinin-induced plasma extravasation, namely prostaglandin E2, ATP, the selective Adenosine A2-Receptor agonist, CGS21680 or the endothelium-derived relaxing factor (as its precursor L-arginine) all greatly enhanced bradykinin-induced plasma extravasation, but produced little or no increase in plasma extravasation administered alone. The data show that sympathetic post-ganglionic neuron-derived mediators may either inhibit or enhance plasma extravasation induced by bradykinin, and we hypothesize that differential release of mediators from the sympathetic post-ganglionic neuron terminal, in response to varying stimuli, regulates local plasma extravasation during inflammation.

Franco Gatta - One of the best experts on this subject based on the ideXlab platform.

Paul Green - One of the best experts on this subject based on the ideXlab platform.

  • modulation of bradykinin induced plasma extravasation in the rat knee joint by sympathetic co transmitters
    Neuroscience, 1993
    Co-Authors: Paul Green, J Luo, Philip H Heller, Jon D. Levine
    Abstract:

    We describe the contribution of various sympathetic post-ganglionic neuron mediators to bradykinin-induced plasma extravasation in the knee joint of the rat. Co-perfusion of the sympathetic post-ganglionic neuron mediators, norepinephrine or neuropeptide Y with bradykinin resulted in diminished plasma extravasation. In contrast, the putative sympathetic post-ganglionic neuron mediators of bradykinin-induced plasma extravasation, namely prostaglandin E2, ATP, the selective Adenosine A2-Receptor agonist, CGS21680 or the endothelium-derived relaxing factor (as its precursor L-arginine) all greatly enhanced bradykinin-induced plasma extravasation, but produced little or no increase in plasma extravasation administered alone. The data show that sympathetic post-ganglionic neuron-derived mediators may either inhibit or enhance plasma extravasation induced by bradykinin, and we hypothesize that differential release of mediators from the sympathetic post-ganglionic neuron terminal, in response to varying stimuli, regulates local plasma extravasation during inflammation.

M R Del Giudice - One of the best experts on this subject based on the ideXlab platform.