Endothelinergic Contractile Hyperreactivity in Rat Contralateral Carotid to Balloon Injury: Integrated Role for ETB Receptors and Superoxide Anion

• Published in: BioMed research international Vol. 2017; no. 2017; pp. 1 - 13
• Main Authors: Moreira, Josimar D., Cardoso, Cristina Ribeiro Barros, do Vale, Bruno N., Gomes, Mayara Santos, Gimenes, Lilian R., Pernomian, Larissa, de Oliveira, Ana M.
• Format: Journal Article
• Language: English
• Published: Cairo, Egypt Hindawi Publishing Corporation 01.01.2017; Hindawi; Hindawi Limited
• Subjects: Angioplasty; Atherosclerosis; Calcium; Calcium channels; Calcium mobilization; Carotid arteries; Chemiluminescence; Contractility; Contraction; Endothelin 1; Endothelin ETB receptors; Endothelins; Endothelium; Hyperreactivity; Hypersensitivity; Injuries; Laboratory animals; Musculoskeletal system; NAD(P)H oxidase; Oxidase; Pharmaceutical sciences; Pharmacology; Pharmacy; Physiology; Rats; Receptors; Rodents; Stents; Superoxide dismutase; Surgery; Tempol; Veins & arteries; Brazil
• ISSN: 2314-6133; 2314-6141
• DOI: 10.1155/2017/3137580

Temporal consequences of neurocompensation to balloon injury on endothelinergic functionality in rat contralateral carotid were evaluated. Rats underwent balloon injury in left carotid and were treated with CP-96345 (NK1 antagonist). Concentration-response curves for endothelin-1 were obtained in contralateral (right) carotid at 2, 8, 16, 30, or 45 days after surgery in the absence or presence of BQ-123 (ETA antagonist), BQ-788 (ETB antagonist), or Tempol (superoxide-dismutase mimic). Endothelin-1-induced calcium mobilization was evaluated in functional assays carried out with BQ-123, BQ-788, or Tempol. Endothelin-1-induced NADPH oxidase-driven superoxide generation was measured by lucigenin chemiluminescence assays performed with BQ-123 or BQ-788. Endothelin-1-induced contraction was increased in contralateral carotid from the sixteenth day after surgery. This response was restored in CP-96345-treated rats. Endothelium removal or BQ-123 did not change endothelin-1-induced contraction in contralateral carotid. This response was restored by BQ-788 or Tempol. Contralateral carotid exhibited an increased endothelin-1-induced calcium mobilization, which was restored by BQ-788 or Tempol. Contralateral carotid exhibited an increased endothelin-1-induced lucigenin chemiluminescence, which was restored by BQ-788. We conclude that the NK1-mediated neurocompensatory response to balloon injury elicits a contractile hyperreactivity to endothelin-1 in rat contralateral carotid by enhancing the muscular ETB-mediated NADPH oxidase-driven generation of superoxide, which activates calcium channels.