| Project/Area Number |
11671840
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Functional basic dentistry
|
|---|
| Research Institution | Setsunan University (2000)
Osaka University (1999) |
|---|
Principal Investigator |
MAEDA Sadaaki Setsunan Univ., Faculty of Pharmaceut.Sci., Professor, 薬学部, 教授 (00135732)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
SAEKI Makio Osaka Univ., Faculty of Dentistry, Research associate, 歯学部, 助手 (30273692)
YOSHIOKA Yasuhiro Setsunan Univ., Faculty of Pharmaceut.Sci., Research associate, 薬学部, 助手 (40330360)
MATSUDA Toshio Osaka Univ., Faculty of Pharmaceut.Sci., Professor, 薬学部, 教授 (00107103)
|
|---|
| Project Period (FY) |
1999 – 2000
|
| Project Status |
Completed (Fiscal Year 2000)
|
| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2000: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1999: ¥2,900,000 (Direct Cost: ¥2,900,000)
|
|---|
| Keywords | imflammation / cultured trigeminal ganglion cell / nitric oxide / bradykinin / pain / intracellular calcium / writhing reaction |
|---|
| Research Abstract |
In primary cultured trigeminal ganglion cells, NOC12, a nitric oxide (NO) donor, potentiated bradykinin (BK)-induced increase in intracellular free calcium concentration ([Ca^<2+>]i). The effect of NOC12 was blocked by carboxy-PTIO (specific NO radical scavenger) and ODQ (guanylate cyclase inhibitor), but not super oxide dismutase. 8-Bromo-cGMP potentiated the rise of [Ca^<2+>]i induced by BK.Both NOC12 and 8-bromo-cGMP did not affect the increase in [Ca^<2+>]i by histamine and carbachol. These results indicate that NO potentiates BK-induced increase in [Ca^<2+>]i by the activation of guanylate cyclase. This also suggests that NO may affect BK-mediated nociceptive responses.
We investigated the effect of NO on kaolin-induced writhing behavior mediated by BK receptors. Intraperitoneal administration of lipopolysaccharide (LPS) in mice increase kaolin-induced writhing reaction, which was inhibited by BK-B2 receptor agonist Hoe140. The increase was inhibited by 2-iminopiperidine, an inducible NO synthase inhibitor. LPS-activated macrophages produced NO in a dose- and time-dependent manner. Pretreatment with 2-iminopiperidine caused a reduction in LPS-stimulated production of NO by peritoneal macrophages. These results indicate that LPS potentiated kaolin-induced writhing through producing NO.
These results suggest that nitric oxide may potentiate pain perception in inflammation.
|
