Different mechanisms of the rabbit pulmonary arterial contraction caused by 5- or 6-hydroxydopamine |
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Authors: | T Katsuragi R Mori T Furukawa |
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Affiliation: | 1. Institute of Advanced Manufacturing Technology, Hefei Institutes of Physical Science, Chinese Academy of Sciences, Changzhou, 213164, China;2. High Magnetic Field Laboratory, Chinese Academy of Sciences, Hefei, 230031, China;1. Research Network NANOTEC–SUT on Advanced Nanomaterials and Characterization, School of Physics, Suranaree University of Technology, Nakhon Ratchasima 30000, Thailand;2. Thailand Center of Excellence in Physics, MHESRI, Bangkok 10400, Thailand;3. Department of Physics, University of Mandalay, Mandalay, Myanmar;4. National Metal and Materials Technology Center, National Science and Technology Development Agency, Pathumthani 12120, Thailand;5. Institute of Nanomaterials Research and Innovation for Energy, Khon Kaen University, Khon Kaen 40002, Thailand;6. Synchrotron Light Research Institute, Muang Nakhon Ratchasima 30000, Thailand;1. ITER Organization, Route de Vinon sur Verdon, 13115 Saint Paul Lez Durance, France;2. AMEC, 31 Parc du Golf, CS 90519, 13596 Aix en Provence, France;3. Westinghouse, Electrique France/Astare, 122 Avenue de Hambourg, 13008 Marseille, France;4. SOGETI High Tech, 180 Rue René Descartes, 13851 Aix en Provence, France |
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Abstract: | The contractile responses of rabbit arterial strips to 5-hydroxydopamine (5-OHDA) or 6-hydroxydopamine (6-OHDA) were assessed in vitro. The 3H efflux from the pulmonary artery after preloading with [3H]noradrenaline was markedly enhanced by 100 microM 5-OHDA or 6-OHDA. In non-superfused strips, 6-OHDA produced a biphasic contraction, an initial small transient and a subsequent large sustained contraction, whereas 5-OHDA elicited a large monophasic contraction. The 6-OHDA-evoked second large contraction was followed by a marked tachyphylaxis after repeated application of the drug. This contraction was greatly diminished by prazosin or cocaine and by pretreatment with reserpine, indicating an indirect action via noradrenaline release. In contrast, the initial contraction caused by 6-OHDA as well as the contraction caused by 5-OHDA was not inhibited by these agents, except prazosin, implying a direct action at the postsynaptic alpha 1-adrenoceptors. In addition, the concentration-response curve for noradrenaline was significantly shifted to the right by pre-addition of 5-OHDA whereas the curve for 5-HT was virtually unaffected. The results thus suggest that 5-OHDA acts as a postsynaptic alpha 1-adrenoceptor agonist. |
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