Detalhes bibliográficos
| Ano de defesa: |
2018 |
| Autor(a) principal: |
Santana, Joice Simões
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| Orientador(a): |
Ferreira, Reginaldo Nassar
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| Banca de defesa: |
Ferreira, Reginaldo Nassar,
Custódio, Carlos Henrique Xavier,
Ferreira, Patrícia Maria,
Colugnati, Diego Basile |
| Tipo de documento: |
Dissertação
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| Tipo de acesso: |
Acesso aberto |
| Idioma: |
por |
| Instituição de defesa: |
Universidade Federal de Goiás
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| Programa de Pós-Graduação: |
Programa de Pós-graduação em Ciências Fisiológicas - Multicêntrico (ICB)
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| Departamento: |
Instituto de Ciências Biológicas - ICB (RG)
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| País: |
Brasil
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| Palavras-chave em Português: |
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| Palavras-chave em Inglês: |
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| Área do conhecimento CNPq: |
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| Link de acesso: |
http://repositorio.bc.ufg.br/tede/handle/tede/10704
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Resumo: |
on the balance of the excitatory and inhibitory synapses, such as gabaergic ones, is responsible for cardiovascular system modulation. The effects of ghrelin, a 28-amino acids peptide, are mediated by subtype 1a of the growth hormone secretagogue receptor (GHSR1a), densely expressed in the sympathetic pre-motor neurons of PVH. Therefore, this work investigated the effects of ghrelin on the control exercised by PVH on cardiovascular system and its relationship with gabaergic activity. For this purpose, mean systemic arterial pressure (PAM) in the femoral artery and pressure in the left cardiac ventricle (LVP) of Wistar rats (250-300 g) were measured by catheterization. Treatment with 100 nL of 0.03 nM ghrelin injected directly into PVH reduced PAM by 40 ± 12 mmHg and the maximum blood pressure in the left cardiac ventricle (LVPmax) by 28 ± 12 mmHg, as well as its derivative as a function of time (LVdP / dTmax), a measure of inotropism, which was reduced by 2051 ± 946 mmHg / s, without causing statistically significant changes in cardiac chronotropism. In contrast, to demonstrate that the effects of ghrelin were mediated by GHS-R1a, the inhibition of this receptor with 100 nL of PF04628935 (0.06 nM) in PVH caused an increase in PAM of 8 ± 3 mmHg and of LVPmax by 29 ± 8 mmHg; in addition to stimulating inotropism, with LVdP / dTmax being elevated at 1449 ± 467 mmHg / s, and chronotropism, with elevated heart rate at 29 ± 12 bpm. Finally, the comparison of its effects with muscimol, a GABAA receptor agonist, demonstrated that ghrelin potentiated the reduction in blood pressure induced by that drug, reducing PAM by 19 ± 5 mmHg, without significantly altering the pressure in the cardiac left ventricle and inotropism. Interestingly, ghrelin promoted na increase in heart rate by 27 ± 12 bpm, after muscimol injection. The present study demonstrated that the ghrelin axis - GHS-R1a in PVH contributes to cardiovascular control and related these effects to interactions with the gabaergic system. |
