HOMEPRODUCTSCOMPANYCONTACTFAQResearchDictionaryPharmaSign Up FREE or Login

Characterization of cardiovascular reflexes evoked by airway stimulation with allylisothiocyanate, capsaicin, and ATP in Sprague-Dawley rats.

Abstract
Acute inhalation of airborne pollutants alters cardiovascular function and evidence suggests that pollutant-induced activation of airway sensory nerves via the gating of ion channels is critical to these systemic responses. Here, we have investigated the effect of capsaicin [transient receptor potential (TRP) vanilloid 1 (TRPV1) agonist], AITC [TRP ankyrin 1 (TRPA1) agonist], and ATP (P2X2/3 agonist) on bronchopulmonary sensory activity and cardiovascular responses of conscious Sprague-Dawley (SD) rats. Single fiber recordings show that allyl isothiocyanate (AITC) and capsaicin selectively activate C fibers, whereas subpopulations of both A and C fibers are activated by stimulation of P2X2/3 receptors. Inhalation of the agonists by conscious rats caused significant bradycardia, atrioventricular (AV) block, and prolonged PR intervals, although ATP-induced responses were lesser than those evoked by AITC or capsaicin. Responses to AITC were inhibited by the TRP channel blocker ruthenium red and the muscarinic antagonist atropine. AITC inhalation also caused a biphasic blood pressure response: a brief hypertensive phase followed by a hypotensive phase. Atropine accentuated the hypertensive phase, while preventing the hypotension. AITC-evoked bradycardia was not abolished by terazosin, the α1-adrenoceptor inhibitor, which prevented the hypertensive response. Anesthetics had profound effects on AITC-evoked bradycardia and AV block, which was abolished by urethane, ketamine, and isoflurane. Nevertheless, AITC inhalation caused bradycardia and AV block in paralyzed and ventilated rats following precollicular decerebration. In conclusion, we provide evidence that activation of ion channels expressed on nociceptive airway sensory nerves causes significant cardiovascular effects in conscious SD rats via reflex modulation of the autonomic nervous system.
AuthorsJ S Hooper, S H Hadley, K F Morris, J W Breslin, J B Dean, T E Taylor-Clark
JournalJournal of applied physiology (Bethesda, Md. : 1985) (J Appl Physiol (1985)) Vol. 120 Issue 6 Pg. 580-91 (Mar 15 2016) ISSN: 1522-1601 [Electronic] United States
PMID26718787 (Publication Type: Journal Article)
CopyrightCopyright © 2016 the American Physiological Society.
Chemical References
  • Air Pollutants
  • Isothiocyanates
  • TRPC Cation Channels
  • Adenosine Triphosphate
  • allyl isothiocyanate
  • Capsaicin
Topics
  • Adenosine Triphosphate (adverse effects, pharmacology)
  • Air Pollutants (adverse effects)
  • Animals
  • Autonomic Nervous System (drug effects, metabolism)
  • Bradycardia (chemically induced, metabolism)
  • Capsaicin (adverse effects, pharmacology)
  • Cardiovascular System (drug effects, metabolism)
  • Isothiocyanates (adverse effects, pharmacology)
  • Male
  • Nerve Fibers, Unmyelinated (metabolism)
  • Rats
  • Rats, Sprague-Dawley
  • Reflex (drug effects)
  • Respiratory System (drug effects, metabolism)
  • Sensory Receptor Cells (drug effects)
  • TRPC Cation Channels (metabolism)

Join CureHunter, for free Research Interface BASIC access!

Take advantage of free CureHunter research engine access to explore the best drug and treatment options for any disease. Find out why thousands of doctors, pharma researchers and patient activists around the world use CureHunter every day.
Realize the full power of the drug-disease research graph!


Choose Username:
Email:
Password:
Verify Password:
Enter Code Shown: