| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Department of Physiology, National Yang-Ming University, Taipei, Taiwan - Republic of China; Department of Physiology, Chung-Shan Medical University, Taichung, Taiwan - Republic of China
2 Department of Physiology, Taipei Medical University, Taipei, Taiwan - Republic of China
3 Department of Pharmacology, National Yang-Ming University, Taipei, Taiwan - Republic of China
4 Department of Physiology, National Yang-Ming University, Taipei, Taiwan - Republic of China
* To whom correspondence should be addressed. E-mail: yrkou{at}ym.edu.tw.
Inhalation of H2O2 is known to evoke bradypnea followed by tachypnea, which are reflexes resulting from stimulation by reactive oxygen species of vagal lung capsaicin-sensitive and myelinated afferents, respectively. This study investigated the pharmacological receptors and chemical mediators involved in triggering these responses. The ventilatory responses to 0.2% aerosolized H2O2 were studied before and after various pharmacological pretreatments in anesthetized rats. The initial bradypneic response was reduced by a transient receptor potential vanilloid 1 (TRPV1) receptor antagonist (capsazepine; 
= -53%) or a P2X purinoceptor antagonist (iso-PPADS; = -47%) and was further reduced by capsazepine and iso-PPADS in combination ( = -78%). The initial bradypneic response was reduced by a cyclooxygenase inhibitor (indomethacin; = -48%), ATP scavengers (apyrase and adenosine deaminase in combination; = -50%) or capsazepine and indomethacin in combination ( = -47%), was further reduced by iso-PPADS and indomethacin in combination ( = -75%) or capsazepine and ATP scavengers in combination ( = -83%), but was not affected by a lipoxygenase inhibitor (nordihydroguaiaretic acid) or by any of the various vehicles. No pretreatment influenced delayed tachypnea. We concluded that 1) the initial bradypneic response to H2O2 results from activation of both TRPV1 and P2X receptors possibly located at terminals of vagal lung capsaicin-sensitive afferent fibers, 2) the functioning of the TRPV1 and P2X receptors in triggering the initial bradypnea are in part mediated through the actions of cyclooxygenase metabolites and ATP, respectively and 3) these mechanisms do not contribute to the H2O2-evoked delayed tachypnea.
This article has been cited by other articles:
|
|
 |
|
  T. Kawahara and J. D. Lambeth Phosphatidylinositol (4,5)-bisphosphate Modulates Nox5 Localization via an N-Terminal Polybasic Region Mol. Biol. Cell, October 1, 2008; 19(10): 4020 - 4031. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. A. Andersson, C. Gentry, S. Moss, and S. Bevan Transient Receptor Potential A1 Is a Sensory Receptor for Multiple Products of Oxidative Stress J. Neurosci., March 5, 2008; 28(10): 2485 - 2494. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. Zhong and D. H. Wang TRPV1 gene knockout impairs preconditioning protection against myocardial injury in isolated perfused hearts in mice Am J Physiol Heart Circ Physiol, September 1, 2007; 293(3): H1791 - H1798. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Burnstock Physiology and Pathophysiology of Purinergic Neurotransmission Physiol Rev, April 1, 2007; 87(2): 659 - 797. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
