Dorsal hippocampus cholinergic and nitrergic neurotransmission modulates the cardiac baroreflex function in rats
Autor: | Luciana Bärg Kuntze, Egidi Mayara Silva Firmino, Davi Campos Lagatta, Nilson C. Ferreira-Junior, Anna B Borges-Assis, Karla Nívea Sampaio, Leonardo B.M. Resstel, Eduardo Akira Fujiwara |
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Rok vydání: | 2018 |
Předmět: |
medicine.drug_class
Cholinergic Agents Baroreflex Pharmacology Nitric Oxide Hippocampus Synaptic Transmission Nitric oxide 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Muscarinic acetylcholine receptor medicine Animals Rats Wistar 030304 developmental biology 0303 health sciences Basal forebrain Chemistry musculoskeletal neural and ocular physiology General Neuroscience Pirenzepine Rats nervous system Acetylcholinesterase inhibitor cardiovascular system Cholinergic 030217 neurology & neurosurgery Acetylcholine circulatory and respiratory physiology medicine.drug |
Zdroj: | The European journal of neuroscienceREFERENCES. 51(4) |
ISSN: | 1460-9568 |
Popis: | Hippocampus is a limbic structure involved in the baroreflex and chemoreflex control that receives extensive cholinergic input from basal forebrain. Hippocampal muscarinic receptors activation by acetylcholine might evoke nitric oxide synthesis, which is an important neuromodulator of cardiovascular responses. Thus, we hypothesize that cholinergic and nitrergic neurotransmission within the DH modulates the baroreflex and chemoreflex function. We have used vasoactive drugs (phenylephrine and sodium nitroprusside), and potassium cyanide infused peripherally to induce, respectively, baroreflex or chemoreflex responses in awake animals. Bilateral injection into the DH of the acetylcholinesterase inhibitor (neostigmine) reduced baroreflex responses. Meanwhile, the non-selective muscarinic receptor antagonist (atropine) or the M1-selective muscarinic receptor antagonist increased baroreflex responses (pirenzepine). Furthermore, the neuronal nitric oxide synthase inhibitor (N-propyl) or the intracellular NO scavenger (carboxy-PTIO) increased baroreflex responses, as well as the selective inhibitor of NO-sensitive guanylyl cyclase (ODQ), increased the baroreflex responses. Besides, bilateral administration of an ineffective dose of a neuronal nitric oxide synthase inhibitor abolished the reduction in the baroreflex responses evoked by an acetylcholinesterase inhibitor. On the other hand, we have demonstrated that hippocampal cholinergic neurotransmission did not influence the chemoreflex function. Taken together, our findings suggest that nNOS-derived nitric oxide in the DH participates in acetylcholine-evoked baroreflex responses. |
Databáze: | OpenAIRE |
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