Activation of ventrolateral medulla neurons by arginine vasopressin via V 1A receptors produces inhibition on respiratory-related hypoglossal nerve discharge in the rat

Ching Wen Chuang, Meng Tzu Cheng, Shu Ju Yang, Ji-Chuu Hwang

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

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 V 1A 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 V 1A receptor antagonist. Our results suggested that AVP may activate neurons located at the VLM and/or rVRG via the AVP V 1A receptor to inhibit respiratory-related HNA and thus to regulate upper airway aperture.

Original languageEnglish
Pages (from-to)144-154
Number of pages11
JournalChinese Journal of Physiology
Volume48
Issue number3
Publication statusPublished - 2005 Sep 30

Fingerprint

Hypoglossal Nerve
Arginine Vasopressin
Neurons
Microinjections
Gallamine Triethiodide
Prone Position
Phrenic Nerve
Hyperoxia
Phentolamine
Urethane
Neurotransmitter Agents
Central Nervous System

Keywords

  • AVP V receptor antagonist
  • Arginine vasopressin (AVP)
  • Blood pressure
  • Hypoglossal nerve discharge
  • Phrenic nerve activity
  • Rats
  • Ventrolateral medulla

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

Activation of ventrolateral medulla neurons by arginine vasopressin via V 1A receptors produces inhibition on respiratory-related hypoglossal nerve discharge in the rat . / Chuang, Ching Wen; Cheng, Meng Tzu; Yang, Shu Ju; Hwang, Ji-Chuu.

In: Chinese Journal of Physiology, Vol. 48, No. 3, 30.09.2005, p. 144-154.

Research output: Contribution to journalArticle

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abstract = "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 V 1A 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 V 1A receptor antagonist. Our results suggested that AVP may activate neurons located at the VLM and/or rVRG via the AVP V 1A receptor to inhibit respiratory-related HNA and thus to regulate upper airway aperture.",
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