Therapeutic efficacy of TBC3711 in monocrotaline-induced pulmonary hypertension

Respir Res. 2011 Jun 23;12(1):87. doi: 10.1186/1465-9921-12-87.

Abstract

Background: Endothelin-1 signalling plays an important role in pathogenesis of pulmonary hypertension. Although different endothelin-A receptor antagonists are developed, a novel therapeutic option to cure the disease is still needed. This study aims to investigate the therapeutic efficacy of the selective endothelin-A receptor antagonist TBC3711 in monocrotaline-induced pulmonary hypertension in rats.

Methods: Monocrotaline-injected male Sprague-Dawley rats were randomized and treated orally from day 21 to 35 either with TBC3711 (Dose: 30 mg/kg body weight/day) or placebo. Echocardiographic measurements of different hemodynamic and right-heart hypertrophy parameters were performed. After day 35, rats were sacrificed for invasive hemodynamic and right-heart hypertrophy measurements. Additionally, histologic assessment of pulmonary vascular and right-heart remodelling was performed.

Results: The novel endothelin-A receptor antagonist TBC3711 significantly attenuated monocrotaline-induced pulmonary hypertension, as evident from improved hemodynamics and right-heart hypertrophy in comparison with placebo group. In addition, muscularization and medial wall thickness of distal pulmonary vessels were ameliorated. The histologic evaluation of the right ventricle showed a significant reduction in fibrosis and cardiomyocyte size, suggesting an improvement in right-heart remodelling.

Conclusion: The results of this study suggest that the selective endothelin-A receptor antagonist TBC3711 demonstrates therapeutic benefit in rats with established pulmonary hypertension, thus representing a useful therapeutic approach for treatment of pulmonary hypertension.

MeSH terms

  • Administration, Oral
  • Animals
  • Antihypertensive Agents / administration & dosage
  • Antihypertensive Agents / pharmacology*
  • Disease Models, Animal
  • Echocardiography, Doppler
  • Endothelin A Receptor Antagonists
  • Fibrosis
  • Hemodynamics / drug effects
  • Hypertension, Pulmonary / chemically induced
  • Hypertension, Pulmonary / diagnostic imaging
  • Hypertension, Pulmonary / drug therapy*
  • Hypertension, Pulmonary / metabolism
  • Hypertension, Pulmonary / physiopathology
  • Hypertrophy, Right Ventricular / diagnostic imaging
  • Hypertrophy, Right Ventricular / drug therapy*
  • Hypertrophy, Right Ventricular / metabolism
  • Hypertrophy, Right Ventricular / physiopathology
  • Isoxazoles / administration & dosage
  • Isoxazoles / pharmacology*
  • Male
  • Monocrotaline*
  • Pulmonary Artery / drug effects
  • Pulmonary Artery / physiopathology
  • Rats
  • Rats, Sprague-Dawley
  • Receptor, Endothelin A / metabolism
  • Sulfones / administration & dosage
  • Sulfones / pharmacology*
  • Time Factors
  • Ventricular Function, Right / drug effects
  • Ventricular Remodeling / drug effects

Substances

  • Antihypertensive Agents
  • Endothelin A Receptor Antagonists
  • Isoxazoles
  • N-(2-acetyl-4,6-dimethylphenyl)-3-(3,4-dimethylisoxazol-5-ylsulfamoyl)thiophene-2-carboxamide
  • Receptor, Endothelin A
  • Sulfones
  • Monocrotaline