| Project/Area Number |
06670730
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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 | Kumamoto University |
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Principal Investigator |
OKUMURA Ken Kumamoto University, School of Medicine Assistant Professor, 医学部, 助教授 (20185549)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1995: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1994: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | Endothelium / Nitric Oxide / L-arginine / Coronary Circulation / L-Arginine |
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| Research Abstract |
To clarify the role of endotheliun-derived nitric oxide (EDNO) on regulation of coronary blood flow, we performed in-vivo study with anesthetized dogs. We have revealed that EDNO is likely to play a role in the regulation of the basal coronary blood flow (Arch int Pharmacodyn 1994 ; 327 : 251-265) , and the myocardial reactive hyperemia is regulated not only by adenosine but also by the EDNO.(Am J Physiol 1992 ; 263 : H8-H14、Cardiovascular Res 1996 in press) We also showed that when NO synthesis is inhibited, adenosine release is increased in response to themyocardial oxygen demand. With this compensatory adenosine release, coronary flow is increased and ventricular function is unaffected. (Am J Physiol 1996 ; 270 : H427-H434) Chronic inhibition of nitric oxide formation with oral administration of L-NAME,L-arginine analogue, blunted coronary reactive hyperemia, but didnot substantially impair the coronary blood flow associated with increased myocardial oxygen requirements produced by atrial pacing. We have revealed that adenosine is likely to play a role in this conpensation. (60th annual meeting of Japanese circulation society, 1996)
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