• Mingyuan Wu, Chao Qin, Robert D Foreman, and Jay P Farber.
• Department of Physiology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73190, USA. mingyuan-wu@ouhsc.edu
• Auton Neurosci. 2007 May 30;133(2):121-7.

AbstractInhalation of ammonia influences the activity of slowly adapting airway receptors (SARs), but the mechanism(s) is uncertain. Release of inflammatory mediators by transient receptor potential vanilloid receptor-1 (TRPV1) containing nerve endings could affect SAR response to ammonia. We examined how sensitization and subsequent desensitization of the TRPV1 by resiniferatoxin (RTX), affected the responses of SARs to inhaled ammonia. In pentobarbital-anesthetized, paralyzed and artificially ventilated rats, the left cervical vagus nerve was exposed, sectioned rostrally, and desheathed. Single fibers of SARs were identified and recorded. Two milliliters of ammonia vapor (from a 30% NH(4)OH solution) was inhaled over 20 s and responses to ammonia were measured. RTX was injected intravenously at 2 microg/Kg. Twenty minutes later, ammonia inhalation was repeated. Isoproterenol (ISO, 100 microg/kg, i.v.) was used in another set of experiments to block possible ammonia-induced bronchoconstriction. Ammonia increased tonic activity of SARs (n=10, P<0.0001), with complex changes in ventilator-related activity. SAR firing rate began to increase 2.3+/-0.2 min after RTX and returned to control levels at 13.6+/-1.4 min (n=10). By 20 min after RTX cardiovascular responses to ammonia were abolished, but effects on SAR activity were essentially unchanged. ISO did not modify the response of SARs to ammonia (n=8). These data suggest that responses of SARs to ammonia in rats do not depend on release of mediators by nerve endings containing TRPV1 and are not secondary to bronchoconstriction. However, when TRPV1 containing nerve endings were initially activated by RTX, the release of mediators may have affected SAR discharges.

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