| Project/Area Number |
08044233
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| Research Category |
Grant-in-Aid for international Scientific Research
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| Allocation Type | Single-year Grants |
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| Section | Joint Research |
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| Research Field |
Kidney internal medicine
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| Research Institution | Tohoku University |
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Principal Investigator |
ITO Sadayoshi Tohoku Univ.2nd Dept.Int Med.Professor., 医学部, 教授 (40271613)
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| Co-Investigator(Kenkyū-buntansha) |
REN Yilin Henry Ford Hospital.Hypertension Research Div. Research Associate., 高血圧血管部門, 助手
CARRETERO Oscar A Henry Ford Hospital.Hypertension Research Div.Professor., 高血圧血管部門, 教授
REN YiLin ヘンリーフォード病院, 高血圧血管部門, 助手
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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 |
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 1997: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1996: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | macula densa / Angiotensin II / Adenosine / afferent-arteriole / tubuloglomerular feedback / Salt intake / GFR / Homeostasis / 輸出細動脈 |
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| Research Abstract |
The macula densa (MD) senses the change in NaCl concentration in the tubular fluid and thereby controls the resistance of the glomerular afferent arteriole (Af-Art), a phenomenon called the tubuloglomerular feedback (TGF). In collaboration with O.A.Carretero at Hypertension Research Division of Henry Ford Hospital, the project. Investigator (SI), studied the TGF directly using an in vitro preparation in which both isolated Af-Art and the MD were microperfused simultaneously.
Role of Angiotensin II (Ang II) in the TGF
When NaCl concentration at the MD is elevated the Af-Art constricts. This predicts that the GFR would decline under high salt intake. However, in normal subjects, high salt intake results in slightly increased GFR.This paradox could be explained by ressetting of the sensitivity of TGF,in which Ang II reportedly plays a rucial role. We indeed observed that increasing the NaCl concentration at the MD induces less constriction of the Af-Art in the absence than in the presence of Ang II.
Role of Adenosine (Ado) in the TGF
Recent studies indicate that ado plays a role in the TGF.We observed that an ado A receptor antagonist altenuates the Af-Art constriction induced by high NaCl at the MD.A low concentration of ado (10^<-8>M) added to the Af-Art perfusate had no effect on basal diameter but greatly augmented the TGF-mediated Af-Art constriction. On the other hand ado (10^<-8>-10^<-6>M) added to the MD perfusate had no effect on Af-Art diameter whether NaCl concentration of the MD perfusate was high or low. This study suggest ado A_1 receptor in the juxtaglomerular interstium is important in TGF.
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