Physiological and genomic consequences of intermittent hypoxia - Selected contribution: Phrenic long-term facilitation requires 5-HT receptor activation during but not following episodic hypoxia

Citation
Dd. Fuller et al., Physiological and genomic consequences of intermittent hypoxia - Selected contribution: Phrenic long-term facilitation requires 5-HT receptor activation during but not following episodic hypoxia, J APP PHYSL, 90(5), 2001, pp. 2001-2006
Citations number
31
Categorie Soggetti
Physiology
Journal title
JOURNAL OF APPLIED PHYSIOLOGY
ISSN journal
87507587 → ACNP
Volume
90
Issue
5
Year of publication
2001
Pages
2001 - 2006
Database
ISI
SICI code
8750-7587(200105)90:5<2001:PAGCOI>2.0.ZU;2-Y
Abstract
Episodic hypoxia evokes a sustained augmentation of respiratory motor outpu t known as long-term facilitation (LTF). Phrenic LTF is prevented by pretre atment with the 5-hydroxytryptamine (5-HT) receptor antagonist ketanserin. We tested the hypothesis that 5-HT receptor activation is necessary for the induction but not maintenance of phrenic LTF. Peak integrated phrenic nerv e activity (integral Phr) was monitored for 1 h after three 5-min episodes of isocapnic hypoxia (arterial PO2 = 40 +/- 2 Torr; 5-min hyperoxic interva ls) in four groups of anesthetized, vagotomized, paralyzed, and ventilated Sprague-Dawley rats [1) control (n = 11), 2) ketanserin pretreatment (2 mg/ kg iv; n = 7), and ketanserin treatment 0 and 45 min after episodic hypoxia (n = 7 each)]. Ketanserin transiently decreased integral Phr, but it retur ned to baseline levels within 10 min. One hour after episodic hypoxia, inte gral Phr was significantly elevated from baseline in control and in the 0- and 45-min posthypoxia ketanserin groups. Conversely, ketanserin pretreatme nt abolished phrenic LTF. We conclude that 5-HT receptor activation is nece ssary to initiate (during hypoxia) but not maintain (following hypoxia) phr enic LTF.