Objective: TGF-β stimulation of cardiac myocytes induces a hypertrophic responsiveness to
β-adrenoceptor stimulation. This study investigates whether this β-adrenoceptor mediated …

These studies were designed to determine the consequences of constitutive overexpression
of ornithine decarboxylase (ODC) in the heart. Induction of ODC is known to occur in …

We investigated whether selective β1-adrenoceptor stimulation causes hypertrophic growth
on isolated ventricular cardiomyocytes from adult rat. As parameters for the induction of …

OBJECTIVES The study investigated whether β-adrenoceptor antagonists augment the
hypertrophic response of cardiomyocytes evoked by norepinephrine. BACKGROUND In …

In isolated cardiomyocytes, hypertrophic responsiveness to β-adrenergic stimulation can be
induced by pre-exposure of the cells to TGF-β. To characterize genes involved in β …

Aims Cardiac hypertrophy by activation of the β-adrenergic receptor (βAR) is mediated more
efficiently by the β1-AR than by the β2-AR. We investigated the signalling mechanism by …

The aim of the present study was to characterize the receptor subtype and the second
messenger involved in the newly discovered hypertrophic effect of β-adrenoceptor …

Transforming growth factor-β1 (TGF-β1) promotes or inhibits cell proliferation and induces
fibrotic processes and extracellular matrix production in numerous cell types. Several …

Background—β1-2-adrenergic receptors (AR) are key regulators of cardiac contractility and
remodeling in response to catecholamines. β3-AR expression is enhanced in diseased …

Increased levels of plasma catecholamine lead to cardiac hypertrophy via the α-, β-
adrenergic receptors, and partially, type 1 angiotensin II (AT 1) receptor. However, it remains …