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Angiotensin II Stimulates Activation of Fos-Regulating Kinase and c-Jun NH₂-Terminal Kinase in Neuronal Cultures from Rat Brain¹

Department of Physiology (X.-C.H., C.S.) and Department of Biochemistry and Molecular Biology (T.D.), College of Medicine, University of Florida, Gainesville, Florida 32610

Address all correspondence and requests for reprints to: Colin Sumners, Department of Physiology, Box 100274, 1600 Southwest Archer Road University of Florida, Gainesville, Florida 32610. E-mail: csumners{at}phys.med.ufl.edu

c-Fos/c-Jun dimers (activating protein-1 transcription factor) are involved in the modulatory actions of angiotensin II (Ang II) on brain norepinephrine neurons, effects mediated via Ang II type 1 (AT₁) receptors. The transcriptional activities of c-Fos and c-Jun can be augmented by Fos-regulating kinase (FRK) and c-Jun NH₂-terminal kinase (JNK), respectively. In this study, we investigated the effects of Ang II on FRK and JNK activities in neurons cultured from newborn rat hypothalamus and brain stem, which include a population of catecholaminergic cells containing AT₁ receptors. Ang II caused time-dependent increases in the activation of FRK and JNK, effects completely inhibited by the AT₁ receptor antagonist losartan but not by the Ang II type 2 (AT₂) receptor blocker PD123,319. The stimulation of FRK activity by Ang II was abolished by the protein kinase C (PKC) inhibitor GF109203X or the calcium chelator BAPTA, but not by inhibition of calmodulin or calcium/calmodulin-dependent protein kinase II. However, the activation of JNK by Ang II was not dependent on PKC or another calcium-dependent mechanism. These data demonstrate that Ang II stimulates activation of FRK and JNK in neuronal cells, actions that may contribute to the neuromodulatory effects of this peptide.

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