| Project/Area Number |
12671816
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Functional basic dentistry
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| Research Institution | TOKYO DENTAL COLLEGE |
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Principal Investigator |
SUZUKI Takashi Tokyo Dental College, Department of Dentistry, Professor, 歯学部, 教授 (10064669)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥2,600,000 (Direct Cost: ¥2,600,000)
Fiscal Year 2001: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2000: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | Hamster / Submandibular ganglion / Angiotensin II / Calcium channel / Calcium current / GTP-binding protein / Protein kinase C / Losartan / アンギオテンシンII脱分極 / 高閾値活性化Ca^<2+>チャネル / L・N型Ca^<2+>電流抑制 / 電位依存性抑制 / G蛋白 |
|---|
| Research Abstract |
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 system. In a previous study, we have shown that AngII, mediated by AT, receptors, inhibits voltage-dependent calcium channels (VDCCs) 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 1uM AngII inhibited Ica by 32.1%. Intracellular dialysis of anti-Gq/11 antibodies attenuated these inhibition. In addition, treatment of protein kinase G (PKC) activator and inhibitor also attenuated the inhibition. I therefore conclude that Ang II inhibits VDCCs via Gq/11-proteins involving in SMG neurons. In addition, such PKC-dependent pathways mediated mainly L-type VDCCs inhibition.
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