• Medientyp: E-Artikel
  • Titel: Chronic Hypertension Switches Irritant‐Induced Pulmonary‐Cardiac Reflexes to Sympathoexcitation
  • Beteiligte: Taylor‐Clark, Tom; Hooper, J Shane
  • Erschienen: Wiley, 2017
  • Erschienen in: The FASEB Journal
  • Sprache: Englisch
  • DOI: 10.1096/fasebj.31.1_supplement.718.1
  • ISSN: 0892-6638; 1530-6860
  • Schlagwörter: Genetics ; Molecular Biology ; Biochemistry ; Biotechnology
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  • Beschreibung: <jats:p>Inhalation of pollutants acutely increases morbidity and mortality in individuals with pre‐existing cardiovascular disease. In these individuals, pollutants cause hazardous tachyarrhythmia and decreased heart rate variability consistent with sympathoexcitation. Nevertheless, in healthy animals and humans, inhalation of pollutants and irritants evokes parasympathetic‐mediated bradycardia. Here, we have compared the changes in blood pressure and the cardiac cycle in normotensive Wistar‐Kyoto rats (WK) and Spontaneously Hypertensive rats (SH) upon inhalation of allyl isothiocyanate (AITC), a selective agonist of TRPA1, the major pollutant‐sensor expressed on airway nociceptive nerves. Studies were performed in conscious, unrestrained 15‐week old rats using radiotelemetry. Resting mean arterial blood pressure were 188 mmHg and 120 mmHg for SH and WK, respectively. Resting heart rates were not different between the strains (~360 bpm). Inhalation of AITC caused substantial bradycardia and AV nodal block in WK, which was prevented by the muscarinic inhibitor atropine. In SH, inhalation of AITC caused bouts of brady‐tachycardia accompanied by both AV block and premature ventricular contractions (PVCs). Atropine prevented the evoked bradycardia and AV block in SH, exposing greater reflex tachycardia. The beta1‐adrenoceptor antagonist atenolol prevented AITC‐evoked tachycardia and PVCs in SH. AITC caused much greater hypertension in SH compared to WK. 24 hour treatment of captopril, the angiotensin converting enzyme inhibitor, normalized blood pressure in SH. Nevertheless, captopril had no effect on AITC‐evoked reflexes in SH. These data indicate that pre‐existing chronic hypertension remodels pollution‐sensitive pulmonary‐cardiac reflexes from parasympathetic towards sympathoexcitation. The remodeled reflex is not dependent on preservation of the hypertension.</jats:p><jats:p><jats:bold>Support or Funding Information</jats:bold></jats:p><jats:p>American Heart Association Grant‐in‐Aid (16GRNT31460004)</jats:p>