ArticleJournal of experimental pharmacology2010
Effects of an oral dose of l-glutamic acid on circulating neurotransmitters: Possible roles of the C1(Ad) and the A5(NA) pontomedullary nuclei.
Article in Journal of experimental pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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6 authors at 1 institution in 1 country.
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Abstract
objectiveInvestigation of the effects of an oral administration of a small dose of l-glutamic acid on the two peripheral sympathetic branches (neural and adrenal) of the autonomic nervous system. RESEARCH DESIGN AND
methodsCirculating neurotransmitters and cardiovascular parameters were assessed in 28 healthy volunteers before and after the administration of 500 mg of l-glutamic acid or placebo.
resultsThe drug triggered a significant and sustained enhancement of the noradrenaline and dopamine circulating levels which were paralleled and positively correlated with the diastolic blood pressure increases. Conversely, both platelet and plasma serotonin showed significant falls throughout the test. Significant positive correlations were registered between noradrenaline, dopamine, and noradrenaline/dopamine ratio versus diastolic blood pressure but not versus systolic blood pressure or heart rate.
conclusionThe above results allowed us to postulate that the drug provoked a significant enhancement of peripheral neural sympathetic activity and the reduction of adrenal sympathetic and parasympathetic drives. Both sympathetic branches are positively correlated with the A5 noradrenergic and the C1 adrenergic pontomedullary nuclei, which interchange inhibitory axons that act at post-synaptic α2 inhibitory autoreceptors. In addition, we discussed the mechanisms able to explain why the drug acted preferentially at the A5 noradrenergic rather than the C1 adrenergic nuclei.
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