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J. Biol. Chem., Vol. 268, Issue 21, 15374-15380, Jul, 1993
KU Knowlton, MC Michel, M Itani, HE Shubeita, K Ishihara, JH Brown and KR Chien
alpha 1-Adrenergic agonists induce a hypertrophic phenotype in cultured
neonatal rat ventricular myocytes. Quantifiable markers of this phenotype
include stimulation of phosphoinositide hydrolysis, transcriptional
induction of atrial natriuretic factor (ANF) gene expression, and an
increase in myocardial cell size. The aim of the present work was to
determine which alpha 1-adrenergic receptor subtype mediates the
acquisition of these parameters of myocardial cell hypertrophy.
Phosphoinositide hydrolysis is inhibited by low concentrations of
5-methylurapidil (log Ki = -8.7) and (+)-niguldipine (log Ki = -10.6). The
alpha-adrenergic receptor-induced increase in transcriptional activation of
an ANF luciferase reporter gene is inhibited over the same range of
concentrations of 5-methylurapidil (log Ki = -8.2) and (+)-niguldipine (log
Ki = -11.2) that inhibit phosphoinositide hydrolysis. In addition, the
increase in cell size that accompanies alpha-adrenergic receptor
stimulation of cultured ventricular myocytes is blocked by similar
concentrations of 5- methylurapidil (log Ki = -8.0) and (+)-niguldipine
(log Ki = -10.6). In contrast, treatment with the alpha 1B selective
antagonist chlorethylclonidine at a concentration of 10 microM had no
effect on the adrenergically mediated induction of ANF luciferase reporter
gene expression or the adrenergically induced increase in myocardial cell
size. These findings demonstrate that pharmacologically identifiable alpha
1A-adrenergic receptors mediate not only the early effects of alpha
1-adrenergic stimulation such as phosphoinositide hydrolysis, but that they
activate the signaling pathways that control transcriptional induction of
the ANF luciferase reporter gene and an increase in myocardial cell size.
Studies using alpha 1-adrenergic receptor cDNAs to delineate and alter the
direct interaction of this receptor subtype with proximal signaling
molecules, e.g. GTP binding proteins, should provide a powerful means of
assessing their role in the induction of the molecular and morphologic
parameters of myocardial cell hypertrophy.
The alpha 1A-adrenergic receptor subtype mediates biochemical, molecular, and morphologic features of cultured myocardial cell hypertrophy
Department of Medicine, University of California, San Diego, School of Medicine, La Jolla 92093-0613.
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