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pubmed-article:1588002pubmed:abstractTextIn order to assess the status of dopamine in the periphery, we submitted rats to sympathectomy (with guanethidine), to hypoxia, and to both, and measured the concentration and turnover of noradrenaline and dopamine in peripheral organs. Sympathectomy decreased noradrenaline content by 96-99% in all the organs tested. In contrast, dopamine content, which was decreased by 90% in the heart, was not significantly changed in the bladder or lungs. Based on dopamine decrease after guanethidine, and on dopamine:noradrenaline ratios in organs, we conclude that in the heart the dopamine is contained mostly in noradrenergic terminals. In other organs it appears to be contained in non-noradrenergic structures. These are found in: the bladder, stomach, lungs, and kidneys, in decreasing importance. We estimated the turnover of noradrenaline by measuring the decrease of its concentration after inhibition of tyrosine hydroxylase with alpha-methyl-p-tyrosine. Among the five organs studied, the turnover of noradrenaline was increased by long-term hypoxia (10% O2, 15 days) in the heart only (+140%). An increase of sympathetic activity during hypoxia was also found in the kidneys and lungs as shown by the increase in turnover of dopamine that was suppressed by sympathectomy. Hypoxia induced large increases in dopamine concentration in the stomach and the lungs (70 and 190% respectively). These increases were not abolished by sympathectomy and we propose that they are related to a chemosensory function of dopamine-containing paraganglia in the stomach and the lung.lld:pubmed
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pubmed-article:1588002pubmed:dateRevised2006-11-15lld:pubmed
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pubmed-article:1588002pubmed:articleTitleResponse of noradrenaline and dopamine to hypoxia and sympathectomy: evidence for an independent dopaminergic reactivity.lld:pubmed
pubmed-article:1588002pubmed:affiliationC.N.R.S., Laboratoire de Physiologie, Lyon, France.lld:pubmed
pubmed-article:1588002pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:1588002pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed