Vasopressin produces inhibition on phrenic nerve activity and apnea through V 1A receptors in the area postrema in rats

Shu Ju Yang, Kun Ze Lee, Chung-Hsin Wu, Kwok-Tung Lu, Ji-Chuu Hwang

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

The area postrema (AP) is the most caudal circumventricular organ in the central nervous system and contains arginine vasopressin (AVP) receptors. To investigate that AVP receptors in the AP might participate in the modulation of respiration, the adult rat was anesthetized with urethane (1.2 g/kg, i.p.), paralyzed, ventilated artificially, and maintained at normocapnia in hyperoxia. The phrenic nerve was separated at C 4 level. Phrenic burst was amplified, filtered, integrated, and then stored in the hard disc via the PowerLab system. Three doses of AVP and an AVP V 1A receptor antagonist, [β-mercapto-β,β-cyclopentamethylenepropionyl 1 ,-O-Me-Tyr 2 ,Arg 8 ]-vasopressin, were microinjected into the AP through a pair of microelectrodes. The moderate and high doses of AVP reduced the PNA to 72 % and 45% of the control (P < 0.05), extended the mean T E from 1.4 s before AVP to 4.0 s and 7.6 s, (P < 0.05), and decrease in BP by 26 and 37 mmHg (P < 0.05), respectively. These significant reductions in PNA and BP and elongation of TE were totally abolished by the pre-treatment of the AVP V 1A receptor antagonist and by application of lidocaine or CoCl 2 at the nucleus tractus solitarius (NTS). Moreover, pulmonary inhibition caused by AVP was significantly attenuated by hypercapnia. These results strongly suggest that AVP V 1A receptors in the AP may participate in the modulation of cardiopulmonary functions through the activation of V 1A receptors and the pathway connected to the NTS. They may also indicate that a putative vasopressinergic pathway has a projection to the AP to alter the excitability of neurons having AVP V 1A receptors and results in an inhibition of cardiopulmonary functions via the connection between the AP and NTS.

Original languageEnglish
Pages (from-to)313-325
Number of pages13
JournalChinese Journal of Physiology
Volume49
Issue number6
Publication statusPublished - 2006 Jan 1

Fingerprint

Area Postrema
Phrenic Nerve
Arginine Vasopressin
Apnea
Vasopressins
Solitary Nucleus
Vasopressin Receptors
Hyperoxia
Hypercapnia
Urethane
Microelectrodes
Lidocaine
Diaphragm
Respiration
Central Nervous System
Neurons
Lung

Keywords

  • Area postrema
  • Arginine vasopressin
  • Phrenic nerve
  • Rat
  • The nucleus of the tractus solitarius

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

@article{bee6fc7d9b1e47a7bed35cdac5ea600e,
title = "Vasopressin produces inhibition on phrenic nerve activity and apnea through V 1A receptors in the area postrema in rats",
abstract = "The area postrema (AP) is the most caudal circumventricular organ in the central nervous system and contains arginine vasopressin (AVP) receptors. To investigate that AVP receptors in the AP might participate in the modulation of respiration, the adult rat was anesthetized with urethane (1.2 g/kg, i.p.), paralyzed, ventilated artificially, and maintained at normocapnia in hyperoxia. The phrenic nerve was separated at C 4 level. Phrenic burst was amplified, filtered, integrated, and then stored in the hard disc via the PowerLab system. Three doses of AVP and an AVP V 1A receptor antagonist, [β-mercapto-β,β-cyclopentamethylenepropionyl 1 ,-O-Me-Tyr 2 ,Arg 8 ]-vasopressin, were microinjected into the AP through a pair of microelectrodes. The moderate and high doses of AVP reduced the PNA to 72 {\%} and 45{\%} of the control (P < 0.05), extended the mean T E from 1.4 s before AVP to 4.0 s and 7.6 s, (P < 0.05), and decrease in BP by 26 and 37 mmHg (P < 0.05), respectively. These significant reductions in PNA and BP and elongation of TE were totally abolished by the pre-treatment of the AVP V 1A receptor antagonist and by application of lidocaine or CoCl 2 at the nucleus tractus solitarius (NTS). Moreover, pulmonary inhibition caused by AVP was significantly attenuated by hypercapnia. These results strongly suggest that AVP V 1A receptors in the AP may participate in the modulation of cardiopulmonary functions through the activation of V 1A receptors and the pathway connected to the NTS. They may also indicate that a putative vasopressinergic pathway has a projection to the AP to alter the excitability of neurons having AVP V 1A receptors and results in an inhibition of cardiopulmonary functions via the connection between the AP and NTS.",
keywords = "Area postrema, Arginine vasopressin, Phrenic nerve, Rat, The nucleus of the tractus solitarius",
author = "Yang, {Shu Ju} and Lee, {Kun Ze} and Chung-Hsin Wu and Kwok-Tung Lu and Ji-Chuu Hwang",
year = "2006",
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language = "English",
volume = "49",
pages = "313--325",
journal = "Chinese Journal of Physiology",
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TY - JOUR

T1 - Vasopressin produces inhibition on phrenic nerve activity and apnea through V 1A receptors in the area postrema in rats

AU - Yang, Shu Ju

AU - Lee, Kun Ze

AU - Wu, Chung-Hsin

AU - Lu, Kwok-Tung

AU - Hwang, Ji-Chuu

PY - 2006/1/1

Y1 - 2006/1/1

N2 - The area postrema (AP) is the most caudal circumventricular organ in the central nervous system and contains arginine vasopressin (AVP) receptors. To investigate that AVP receptors in the AP might participate in the modulation of respiration, the adult rat was anesthetized with urethane (1.2 g/kg, i.p.), paralyzed, ventilated artificially, and maintained at normocapnia in hyperoxia. The phrenic nerve was separated at C 4 level. Phrenic burst was amplified, filtered, integrated, and then stored in the hard disc via the PowerLab system. Three doses of AVP and an AVP V 1A receptor antagonist, [β-mercapto-β,β-cyclopentamethylenepropionyl 1 ,-O-Me-Tyr 2 ,Arg 8 ]-vasopressin, were microinjected into the AP through a pair of microelectrodes. The moderate and high doses of AVP reduced the PNA to 72 % and 45% of the control (P < 0.05), extended the mean T E from 1.4 s before AVP to 4.0 s and 7.6 s, (P < 0.05), and decrease in BP by 26 and 37 mmHg (P < 0.05), respectively. These significant reductions in PNA and BP and elongation of TE were totally abolished by the pre-treatment of the AVP V 1A receptor antagonist and by application of lidocaine or CoCl 2 at the nucleus tractus solitarius (NTS). Moreover, pulmonary inhibition caused by AVP was significantly attenuated by hypercapnia. These results strongly suggest that AVP V 1A receptors in the AP may participate in the modulation of cardiopulmonary functions through the activation of V 1A receptors and the pathway connected to the NTS. They may also indicate that a putative vasopressinergic pathway has a projection to the AP to alter the excitability of neurons having AVP V 1A receptors and results in an inhibition of cardiopulmonary functions via the connection between the AP and NTS.

AB - The area postrema (AP) is the most caudal circumventricular organ in the central nervous system and contains arginine vasopressin (AVP) receptors. To investigate that AVP receptors in the AP might participate in the modulation of respiration, the adult rat was anesthetized with urethane (1.2 g/kg, i.p.), paralyzed, ventilated artificially, and maintained at normocapnia in hyperoxia. The phrenic nerve was separated at C 4 level. Phrenic burst was amplified, filtered, integrated, and then stored in the hard disc via the PowerLab system. Three doses of AVP and an AVP V 1A receptor antagonist, [β-mercapto-β,β-cyclopentamethylenepropionyl 1 ,-O-Me-Tyr 2 ,Arg 8 ]-vasopressin, were microinjected into the AP through a pair of microelectrodes. The moderate and high doses of AVP reduced the PNA to 72 % and 45% of the control (P < 0.05), extended the mean T E from 1.4 s before AVP to 4.0 s and 7.6 s, (P < 0.05), and decrease in BP by 26 and 37 mmHg (P < 0.05), respectively. These significant reductions in PNA and BP and elongation of TE were totally abolished by the pre-treatment of the AVP V 1A receptor antagonist and by application of lidocaine or CoCl 2 at the nucleus tractus solitarius (NTS). Moreover, pulmonary inhibition caused by AVP was significantly attenuated by hypercapnia. These results strongly suggest that AVP V 1A receptors in the AP may participate in the modulation of cardiopulmonary functions through the activation of V 1A receptors and the pathway connected to the NTS. They may also indicate that a putative vasopressinergic pathway has a projection to the AP to alter the excitability of neurons having AVP V 1A receptors and results in an inhibition of cardiopulmonary functions via the connection between the AP and NTS.

KW - Area postrema

KW - Arginine vasopressin

KW - Phrenic nerve

KW - Rat

KW - The nucleus of the tractus solitarius

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