nNOS Gene Deletion Exacerbates Pathological Left Ventricular Remodeling and Functional Deterioration After Myocardial Infarction | Zendy

Dana Dawson | Zendy; Craig A. Lygate | Zendy; Mei-Hua Zhang | Zendy; Karen Hulbert | Zendy; Stefan Neubauer | Zendy; Barbara Casadei | Zendy

Open Access

nNOS Gene Deletion Exacerbates Pathological Left Ventricular Remodeling and Functional Deterioration After Myocardial Infarction

Author(s) -

Dana Dawson,

Craig A. Lygate,

Mei-Hua Zhang,

Karen Hulbert,

Stefan Neubauer,

Barbara Casadei

Publication year - 2005

Publication title -

circulation

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 7.795

H-Index - 607

eISSN - 1524-4539

pISSN - 0009-7322

DOI - 10.1161/circulationaha.105.539437

Subject(s) - dobutamine , medicine , contractility , preload , cardiology , inotrope , myocardial infarction , ventricular remodeling , basal (medicine) , hemodynamics , insulin

The neuronal isoform of nitric oxide synthase (nNOS) has been implicated in the regulation of basal and beta-adrenergic inotropy in normal and chronically infarcted hearts. Furthermore, myocardial nNOS expression and activity increase in failing hearts, raising the possibility that nNOS may influence left ventricular (LV) remodeling progression and functional deterioration after myocardial infarction (MI).

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research