Roles of brain nitric oxide and prostaglandins in the regulation of central sympatho-adrenomedullary outflow in rats
| Project/Area Number |
08672614
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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 |
応用薬理学・医療系薬学
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| Research Institution | Kochi Medical School |
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Principal Investigator |
YOKOTANI Kunihiko Kochi Medical School, Dept.of Pharmacology, Associate Professor, 医学部, 助教授 (30174858)
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1997: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1996: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | Sympathetic nerve / Adrenal medulla / Adrenaline / Noradrenaline / Prostaglandin / Thromboxane A2 / Nitric oxide / Acid secretion / 一酸化窒 / インドメタシン / NO合成酵素阻害薬 / オキシヘモグロビン |
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| Research Abstract |
We already reported that intracerebroventricularly (i.c.v.) administered interleukin-1beta (IL-1beta) inhibits vagally activated gastric acid secretion by activation of central prostaglandin (PG)-mediated sympathetic outflow (Eur.J.Pharmacol., 1995). I.c.v. administered PGE^2 also activates central sympathetic outflow through activation of brain EP3 receptors (Br.J.Pharmacol., 1995 ; 1996). In the present experiments, we examined possible roles of central nitric oxide (NO) in IL-1beta-mediated central activation of sympathetic outflow using male Wistar rats anesthetized with urethane. (1) I.c.v.administered IL-1beta elevated plasma noradrenaline (NA) levels. This IL-1beta-mediated response was abolished by i.c.v.administered 1-NAME (NO synthase inhibitor), oxyhemoglobin (NO scavenger), and indomethacin (cyclooxygenase inhibitor), (2) I.c.v.administered NO donors, sodium nitroprusside and 3-morpholinosydnonimine (SIN-1), inhibited vagally stimulated gastric acid secretion. This response was abolished by i.c.v.administered indomethacin, splanchnectomy and intramuscularly administered phentolamine, SIN-1 elevated plasma levels of adrenaline (Ad) and NA (Ad>>NA). SIN-1-mediated elevation of Ad and NA was abolished by intracerebroventricular pretreatment with indomethacin. On the other hand, intracerebroventricular pretreatment with thromboxane A2 synthase inhibitor, furegrelate, only abolished SIN-1-induced Ad elevation. These results indicate that central NO activates central sympatho-adrenomedullary system. I.c.v.administered IL-1beta activates central sympathetic outflow through NO-PG (E2) pathway and central thromboxane A2 activates central adrenomedullary pathways.
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Report
(3 results)
Research Products
(9 results)
