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Activation of ventrolateral medulla neurons by arginine vasopressin via V1A receptors produces inhibition on respiratory-related hypoglossal nerve discharge in the rat.

Authors: Chuang, CW  Cheng, MT  Yang, SJ  Hwang, JC 
Citation: Chuang CW, etal., Chin J Physiol. 2005 Sep 30;48(3):144-54.
Pubmed: (View Article at PubMed) PMID:16304841

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.

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CRRD Object Information
CRRD ID: 2300377
Created: 2008-09-16
Species: All species
Last Modified: 2008-09-16
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.