Gene/Protein
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Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
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Target Concepts:
Gene/Protein
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Query: UMLS:C0242706 (
hyperoxia
)
5,219
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Arginine vasopressin
(
AVP
) is an important neurohormone in the regulation of many aspects of central nervous system, yet its modulation on the respiratory function remains largely unknown. The aims of this study were to investigate the modulation of phrenic (PNA) and hypoglossal nerve activity (HNA) by central administration of
AVP
and to identify the involvement of
AVP
V1A receptors in this modulation. Animals were anesthetized with urethane (1.2 g/kg, i.p.), paralyzed with gallamine triethiodide (5 mg/kg, i.v.), and artificially ventilated. The rat was then placed on a stereotaxic apparatus in a prone position. PNA and HNA were monitored at normocapnia in
hyperoxia
. Microinjection of
AVP
into the medial ventrolateral medulla (VLM) and/or rostral ventral respiratory group (rVRG) produced a dose-dependent inhibition on both PNA and HNA, whereas the microinjection of
AVP
into the region of lateral VLM resulted in a similar inhibition of these nerve activities and a pressor response. Systemic administration of phentolamine abolished the pressor effect but did not affect the inhibition of PNA and HNA evoked by
AVP
injection into the lateral VLM and/or rVRG, suggesting that
AVP
-induced inhibition of PNA and HNA was not due to the side effect of pressor response. These cardiopulmonary modulations were totally abolished by the central pretreatment of
AVP
V1A receptor antagonist. Our results suggested that
AVP
may activate neurons located at the VLM and/or rVRG via the
AVP
V1A receptor to inhibit respiratory-related HNA and thus to regulate upper airway aperture.
...
PMID:Activation of ventrolateral medulla neurons by arginine vasopressin via V1A receptors produces inhibition on respiratory-related hypoglossal nerve discharge in the rat. 1630 41