Hypoxia-induced hypotension elicits adenosine-dependent phrenic long-term facilitation after carotid denervation.

Hypoxia-induced hypotension elicits adenosine-dependent phrenic long-term facilitation after carotid denervation. Exp Neurol. 2020 Jul 28;:113429 Authors: Perim RR, Kubilis PS, Seven YB, Mitchell GS 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 rats (CBX) via a distinct, but unknown mechanism. We hypothesized that exaggerated hypoxia-induced hypotension after CBX, leading 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. PMID: 32735873 [PubMed - as supplied by publisher]
Source: Experimental Neurology - Category: Neurology Authors: Tags: Exp Neurol Source Type: research

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This article is protected by copyright. All rights reserved. PMID: 30689208 [PubMed - as supplied by publisher]
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