Angiotensin II-induced inhibition of calcium currents via Gq/11-protein involving protein kinase C in hamster submandibular ganglion neurons

  • Yamada E
  • Endoh T
  • Suzuki T
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Angiotensin II (AngII) is one of the most important vasoconstrictive hormones but is also known to act as a neuromodulator and a neurotransmitter in the central and peripheral nervous systems. In a previous study, we have shown that AngII, mediated by AT1receptors, inhibits voltage-dependent calcium channel (VDCC) currents (ICa) via G-proteins in submandibular ganglion (SMG) neurons. In this study, we further characterized the signal transduction of AngII-induced inhibition of ICa. Application of 1 μM AngII inhibited ICaby 32.1±2.7% (mean±S.E.M., n=9). Intracellular dialysis of anti-Gq/11antibodies attenuated these inhibition (8.8±1.3%, n=6). In addition, treatment of protein kinase C (PKC) activator and inhibitor also attenuated these inhibition (8.0±0.9 and 9.8±0.9%, n=6 and 9, respectively). We therefore conclude that AngII inhibits VDCC via Gq/11-proteins involving in SMG neurons. In addition, such PKC-dependent pathways mediated mainly L-type VDCC inhibition. © 2002 Elsevier Science Ireland Ltd and the Japan Neuroscience Society. All rights reserved.

Author-supplied keywords

  • AT1receptor
  • Angiotensin II
  • G-protein-coupled receptor superfamily
  • Parasympathetic ganglion
  • Signal transduction pathway
  • Voltage-gated calcium channels

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  • Emiko Yamada

  • Takayuki Endoh

  • Takashi Suzuki

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