RhoA/ROCK signaling and pleiotropic α1A-adrenergic receptor regulation of cardiac contractility.

ABSTRACT:

Aims

To determine the mechanisms by which the α1A-adrenergic receptor (AR) regulates cardiac contractility.

Background

We reported previously that transgenic mice with cardiac-restricted α1A-AR overexpression (α1A-TG) exhibit enhanced contractility but not hypertrophy, despite evidence implicating this Gαq/11-coupled receptor in hypertrophy.

Methods

Contractility, calcium (Ca(2+)) kinetics and sensitivity, and contractile proteins were examined in cardiomyocytes, isolated hearts and skinned fibers from α1A-TG mice (170-fold overexpression) and their non-TG littermates (NTL) before and after α1A-AR agonist stimulation and blockade, angiotensin II (AngII), and Rho kinase (ROCK) inhibition.

Results

Hypercontractility without hypertrophy with α1A-AR overexpression

SUBMITTER: Yu ZY 

PROVIDER: S-EPMC4053326 | biostudies-literature | 2014

REPOSITORIES: biostudies-literature