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(Received for publication, November 15, 1996, and in revised form, January 23, 1997)
From the The subunit composition of angiotensin
AT1 receptor-activated G protein was identified by
using antisense oligonucleotide injection into the nucleus of rat
portal vein myocytes. In these cells, we have previously shown that
increases in the cytoplasmic calcium concentration
([Ca2+]i) induced by activation of angiotensin
AT1 receptors were dependent on extracellular
Ca2+ entry by L-type Ca2+ channels and
subsequent Ca2+-induced Ca2+ release from the
intracellular stores. The angiotensin AT1
receptor-activated increases in [Ca2+]i were
selectively inhibited by injection of antisense oligonucleotides
directed against the mRNAs coding for the
Volume 272, Number 15,
Issue of April 11, 1997
pp. 10095-10102
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.
13
1
3 Couples the
Angiotensin AT1A Receptor to Increases in Cytoplasmic
Ca2+ in Rat Portal Vein Myocytes
,
,
Laboratoire de Physiologie Cellulaire et
Pharmacologie Moléculaire, CNRS ESA 5017, Université de
Bordeaux II, 146 rue Léo Saignat, 33076 Bordeaux Cedex, France
and the ¶ Institut für Pharmakologie, Freie
Universität Berlin, Thielallee 69/73,
14195 Berlin, Federal Republic of Germany
13, 
1, and 
3 subunits. A correlating
reduction in G13, G1, and G3 protein expression was confirmed by
immunocytochemistry. In addition, anti-13 antibody and
synthetic peptide corresponding to the carboxyl terminus of the
G13 subunit inhibited, in a
concentration-dependent manner, the angiotensin
AT1 receptor-mediated Ca2+ response. Reverse
transcription-polymerase chain reaction analysis showed that only the
angiotensin AT1A receptor was expressed in rat portal vein
smooth muscle. Furthermore, injection of anti-AT1A oligonucleotides selectively inhibited the angiotensin II-induced increase in [Ca2+]i. We conclude that the
receptor-activated signal leading to increases in
[Ca2+]i is transduced by the heterotrimeric
G13 protein composed of
13/1/3 subunits and that
the carboxyl terminus of the G13 subunit interacts with
the angiotensin AT1A receptor.
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