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The Journal of Neuroscience, July 15, 2002, 22(14):5823-5832

Sympathoexcitation by Bradykinin Involves Ca²⁺-Independent Protein Kinase C

Thomas Scholze, Eugenia Moskvina, Martina Mayer, Herwig Just, Helmut Kubista, and Stefan Boehm

Department of Pharmacology, University of Vienna, A-1090 Vienna, Austria

Bradykinin has long been known to excite sympathetic neurons via B₂ receptors, and this action is believed to be mediated by an inhibition of M-currents via phospholipase C and inositol trisphosphate-dependent increases in intracellular Ca²⁺. In primary cultures of rat superior cervical ganglion neurons, bradykinin caused an accumulation of inositol trisphosphate, an inhibition of M-currents, and a stimulation of action potential-mediated transmitter release. Blockade of inositol trisphosphate-dependent signaling cascades failed to affect the bradykinin-induced release of noradrenaline, but prevented the peptide-induced inhibition of M-currents. In contrast, inhibition or downregulation of protein kinase C reduced the stimulation of transmitter release, but not the inhibition of M-currents, by bradykinin. In cultures of superior cervical ganglia, classical (, I, II), novel (, ), and atypical () protein kinase C isozymes were detected by immunoblotting. Bradykinin induced a translocation of Ca²⁺-independent protein kinase C isoforms ( and ) from the cytosol to the membrane of the neurons, but left the cellular distribution of other isoforms unchanged. This activation of Ca²⁺-independent protein kinase C enzymes was prevented by a phospholipase C inhibitor. The bradykinin-dependent stimulation of noradrenaline release was reduced by inhibitors of classical and novel protein kinase C isozymes, but not by an inhibitor selective for Ca²⁺-dependent isoforms. These results demonstrate that bradykinin B₂ receptors are linked to phospholipase C to simultaneously activate two signaling pathways: one mediates an inositol trisphosphate- and Ca²⁺-dependent inhibition of M-currents, the other one leads to an excitation of sympathetic neurons independently of changes in M-currents through an activation of Ca²⁺-insensitive protein kinase C.

Key words: rat superior cervical ganglion neurons; noradrenaline release; bradykinin; M-type K⁺ channels; protein kinase C; phospholipase C

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Copyright © 2002 Society for Neuroscience  0270-6474/02/22145823-10$05.00/0

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