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Effects of an oral dose of l-glutamic acid on circulating neurotransmitters: Possible roles of the C(1)(Ad) and the A(5)(NA) pontomedullary nuclei
OBJECTIVE: Investigation 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 METHODS: Circulating neurotransmitters and cardiovascular parameters were assessed...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove Medical Press
2010
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4863285/ https://www.ncbi.nlm.nih.gov/pubmed/27186090 |
Sumario: | OBJECTIVE: Investigation 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 METHODS: Circulating neurotransmitters and cardiovascular parameters were assessed in 28 healthy volunteers before and after the administration of 500 mg of l-glutamic acid or placebo. RESULTS: The 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. CONCLUSION: The 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 A(5) noradrenergic and the C(1) adrenergic pontomedullary nuclei, which interchange inhibitory axons that act at post-synaptic α(2) inhibitory autoreceptors. In addition, we discussed the mechanisms able to explain why the drug acted preferentially at the A(5) noradrenergic rather than the C(1) adrenergic nuclei. |
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