6 Papers
183 Citations
J. Luo is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Extravasation & Bradykinin. The author has an hindex of 5, co-authored 6 publications.
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Papers
Further substantiation of a significant role for the sympathetic nervous system in inflammation
TL;DR: It is shown that bradykinin is able to release norepinephrine in the knee-joint, indicating action on the sympathetic postganglionic neuron, and substantial additional evidence supporting a significant contribution of the sympatheticPostganglionics neuron terminal to inflammatory plasma extravasation is provided.
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Modulation of bradykinin-induced plasma extravasation in the rat knee joint by sympathetic co-transmitters
TL;DR: The data show that sympathetic post-ganglionic neuron-derived mediators may either inhibit or enhance plasma extravasation induced by bradykinin, and it is hypothesize that differential release of mediators from the sympatheticPost-gangLionic neuron terminal, in response to varying stimuli, regulates local plasmaExtravasation during inflammation.
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Neurogenic and non-neurogenic mechanisms of plasma extravasation in the rat
TL;DR: It was found that bradykinin-induced plasma extravasation was antagonized stereospecifically by the inhibitor of endothelium-derived relaxing factor synthesis, NG-monomethyl-L-arginine, which exerted an influence on non-neurogenic plasmaExtravasation.
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Trypsin enhances sympathetic neuron-dependent plasma extravasation in the rat knee joint.
TL;DR: The data suggests that 6-hydroxydopamine not only releases mediators from the sympathetic neuron that produce plasmaExtravasation, but also an inhibitor(s) of plasma extravasation that is peptide in nature.
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Effect of E-type prostaglandins on bradykinin-induced plasma extravasation in the knee joint of the rat.
TL;DR: It is demonstrated that in the rat knee joint, misoprostol and enisoprost have different pharmacological actions compared to their parent compound, prostaglandin E1 and to prostaglandsin E2.
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