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We have recently shown that vasoactive peptides such as angiotensin II (Ang II) and endothelin-1 (ET-1) increased the expression of [G.sub.i] proteins and proliferation of A10 vascular smooth muscle cells (VSMC) through MAP kinase/PI3 kinase pathways. The present study was undertaken to examine the implication of growth factor receptor activation in Ang II-induced enhanced expression of [G.sub.i] proteins and proliferation of A10 VSMC and to further investigate the underlying mechanisms responsible for these increases. Cell proliferation was determined by [³H]thymidine incorporation, and the expression of [G.sub.i] proteins and the phosphorylation of ERK1/2 and epidermal growth factor receptor (EGFR) was determined by Western blotting. Treatment of A10 VSMC with Ang II enhanced the expression of [G.sub.i] proteins, which was attenuated by Ang II [AT.sub.1] receptor antagonist but not by [AT.sub.2] receptor antagonist. The inhibitor of EGFR also attenuated the enhanced expression of [G.sub.i] proteins induced by Ang II to control levels. In addition, Ang II enhanced the phosphorylation of EGFR in A10 VSMC, and this was restored to control levels by the EGFR inhibitor and antioxidants. Furthermore, Ang II also augmented the proliferation and ERK1/2 phosphorylation of A10 VSMC, which were restored to control levels by the EGFR inhibitor. These data suggest that the Ang II-induced increase in oxidative stress transactivates EGFR, which through MAP kinase signaling may contribute to the enhanced expression of [G.sub.i] proteins and thereby to the increased proliferation of A10 VSMC. Key words: Ang II, EGFR, ERK1/2, [G.sub.i] proteins, oxidative stress, VSMC proliferation. Nous avons montre recemment que les peptides vasoactifs tels que l'angiotensine II (Ang II) et l'endotheline-1 (ET-1) augmentent l'expression des proteines [G.sub.i] et la proliferation des cellules du muscle lisse vasculaire (CMLV) A10, et ce, par les voies des MAP kinases/PI3 kinases. La presente etude a eu pour but d'examiner le role de l'activation du recepteur du facteur des croissance dans l'augmentation par Ang II de l'expression des proteines [G.sub.i] et de la proliferation des CMLV A10, ainsi que d'etudier plus en detail les meecanismes a l'origine de ces augmentations. Nous avons mesure la proliferation des cellules par incorporation de [³H]thymidine et determine par immunobuvardage de type western l'expression des proteines [G.sub.i] ainsi que la phosphorylation des recepteurs de la proteine ERK1/2 et du facteur de croissance epidermique (R-EGF). Le traitement des CMLV A10 par Ang II a stimule l'expression des proteines [G.sub.i], qui a ete attenuee par l'antagoniste du recepteur [AT.sub.1] de l'Ang II, mais pas par l'antagoniste du recepteur [AT.sub.2]. De plus, l'inhibiteur du REGF a aussi diminuee au niveau des valeurs teemoins l'augmentation par Ang II de l'expression des proteines [G.sub.i].Dememe, l'Ang II a stimule; la phosphorylation du R-EGF dans les CMLV A10, laquelle a ete ramenee aux taux teemoins par l'inhibiteur du R-EGF ainsi que par des antioxydants. L'Ang II a aussi augmented la proliferation et la phosphorylation de la proteine ERK1/2 des CMLV A10, lesquelles ont ete rameneees aux valeurs temoins par l'inhibiteur du R-EGF. Ces resultants donnent a penser que l'augmentation du stress oxydatif par l'Ang II transactive le R-EGF qui, par la voie de signalisation des MAP kinases, pourrait jouer un role dans l'augmentation de l'expression des proteines [G.sub.i] et, par consequent, dans l'augmentation de la proliferation des CMLV A10. Mots-cles: Ang II, EGFR, ERK1/2, proteines [G.sub.i], stress oxydatif, proliferation des CMLV. [Traduit par la Redaction] doi: 10.1139/Y09-089, Introduction Guanine nucleotide regulatory proteins (G proteins) are a family of GTP-binding proteins that play an important role in the regulation of a variety of signal transduction systems, including the [...]