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Please use this identifier to cite or link to this item: http://ir.ncue.edu.tw/ir/handle/987654321/11999

Title: Activation of Ventrolateral Medulla Neurons by Arginine Vasopressin via V1A Receptors Produces Inhibition on Respiratory-Related Hypoglossal Nerve Discharge in the Rat
Authors: Chuang, Ching-Wen;Cheng, Meng‐Tzu;Yang, Shu-Ju;Hwang, Ji-Chuu
Contributors: 生物學系
Keywords: Arginine vasopressin (AVP);AVP V1A receptor antagonist;Ventrolateral medulla;Phrenic nerve activity;Hypoglossal nerve discharge;Blood pressure;Rats
Date: 2005-09
Issue Date: 2012-07-03T02:45:12Z
Publisher: The Chinese Physiological Society & Airiti Press
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 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 AVPinduced
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.
Relation: The Chinese Journal of Physiology, 48(3): 144-154
Appears in Collections:[Department of Biology] Periodical Articles

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