Hypoxia-induced hypotension elicits adenosine-dependent phrenic long-term facilitation after carotid denervation.
Exp Neurol
; 333: 113429, 2020 11.
Article
em En
| MEDLINE
| ID: mdl-32735873
ABSTRACT
Moderate acute intermittent hypoxia (AIH) elicits a persistent, serotonin-dependent increase in phrenic amplitude, known as phrenic long-term facilitation (pLTF). Although pLTF was originally demonstrated by carotid sinus nerve stimulation, AIH still elicits residual pLTF in carotid denervated (CBX) rats via a distinct, but unknown mechanism. We hypothesized that exaggerated hypoxia-induced hypotension after carotid denervation leads to greater spinal tissue hypoxia and extracellular adenosine accumulation, thereby triggering adenosine 2A receptor (A2A)-dependent pLTF. Phrenic activity, arterial pressure and spinal tissue oxygen pressure were measured in anesthetized CBX rats. Exaggerated hypoxia-induced hypotension after CBX was prevented via intravenous phenylephrine; without the hypotension, spinal tissue hypoxia during AIH was normalized, and residual pLTF was no longer observed. Spinal A2A (MSX-3), but not serotonin 2 receptor (5-HT2) inhibition (ketanserin), abolished residual pLTF in CBX rats. Thus, pLTF regulation may be altered in conditions impairing sympathetic activity and arterial pressure regulation, such as spinal cord injury.
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Base de dados:
MEDLINE
Assunto principal:
Nervo Frênico
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Corpo Carotídeo
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Potenciação de Longa Duração
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Hipotensão
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Hipóxia
Idioma:
En
Ano de publicação:
2020
Tipo de documento:
Article