Abstract
Previous studies have shown that patients with Takotsubo syndrome (TS) have supranormal nitric oxide signaling, and post-mortem studies of TS heart samples revealed nitrosative stress. Therefore, we first showed in a female rat model that isoproterenol induces TS-like echocardiographic changes, evidence of nitrosative stress, and consequent activation of the energy-depleting enzyme poly(ADP-ribose) polymerase-1. We subsequently showed that pre-treatment with an inhibitor of poly(ADP-ribose) polymerase-1 ameliorated contractile abnormalities. These findings thus add to previous reports of aberrant β-adrenoceptor signaling (coupled with nitric oxide synthase activation) to elucidate mechanisms of impaired cardiac function in TS and point to potential methods of treatment.
Original language | English |
---|---|
Pages (from-to) | 213-226 |
Number of pages | 14 |
Journal | JACC: Basic to Translational Science |
Volume | 3 |
Issue number | 2 |
Early online date | 18 Apr 2018 |
DOIs | |
Publication status | Published - Apr 2018 |
Keywords
- Takotsubo cardiomyopathy
- myocardial inflammation
- oxidative stress
- poly(ADP-Ribose) polymerase-1