| Project/Area Number |
01570463
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Tohoku University |
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Principal Investigator |
KIMURA Tokihisa The 2nd Dept. of Int. Med. Lecturer, 医学部附属医院, 講師 (00004945)
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| Co-Investigator(Kenkyū-buntansha) |
SHOJI Masaru The 2nd Dept. of Int. Med. Assistant, 医学部附属医院, 助手 (10226300)
OTA Kozo The 2nd Dept. of Int. Med. Assistant, 医学部附属病院, 助手 (10185267)
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| Project Period (FY) |
1989
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| Project Status |
Completed (Fiscal Year 1990)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1990: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1989: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | Vasopressin / GABA / Angiotensin / Acethylcholine / Central nervous system / Osmoregulation / Hemorrhagic shock / 浸透圧調節 / 抗利尿ホルモン / 水電解質代謝 / 血圧調節 / ナトリウム利尿ホルモン / 間脳下垂体 |
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| Research Abstract |
(1) Effects of GABA on AVP release and cardiovascular function in response to either angiotensin II (Ang II), carbachol (CB) or hypertonic saline given intracerebroventricularly (icv) as well as to either HS given iv or hemorrhagic shock.
Ang II and CB increased plasma AVP and mean arterial blood pressure (MABP), but GABA never affected these changes. On the other hand, increases in MABP and plasma AVP produced by HS given icv were apparently attenuated by GABA. HS given iv stimulated AVP release without increased MABP, and GABA attenuated AVP release. Increased AVP release induced by hemorrhagic shock was not suppressed by GABA. These results showed that gabanergic neurons may inhibit AVP release and an increase in MABP mediated by osmotic challenge, but not the responses to Ang II, CB and hemorrhagic shock.
(2) Effects of endothelin (ET) given icv on AVP release and cardiovascular function.
ET in the relatively high dose stimulated AVP and ANP release and increased MABP, but not these release in the low dose except increased MABP. These results showed that ET centrally increased blood pressure via increases in AVP release and sympathetic outflow.
ses in AVP release and sympathetic outflow.
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