1989 Fiscal Year Final Research Report Summary
Biochemistry and Pathophysiology of the Kinin-tensin enzyme system
| Project/Area Number |
62480221
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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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 | Fukuoka University |
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Principal Investigator |
ARAKAWA Kikuo Fukuoka University, School of Med. Professor, 医学部, 教授 (90078783)
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| Co-Investigator(Kenkyū-buntansha) |
SASAGURI Manabu Fukuoka University, School of Med., Lecturer, 医学部, 講師 (00178675)
IDEISHI Munehito Fukuoka University, School of Med., Lecturer, 医学部, 講師 (20131807)
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| Project Period (FY) |
1987 – 1989
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| Keywords | Kinin / Angiotensin / Kallikrein / Captopril / Nafamostat / Myocardial infarction / Arteriosclerosis obliterans / Hydroxyproline |
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| Research Abstract |
Biochemical and pathophysiological nature of kinin-tensin enzyme system was investigated in this project.
Rat submandibular gland and human urinary kallikrein were also capable of forming angiotengin II in addition to the well known product kinin. In the rat hindlimb perfusion experiment, angiotensin II was formed in the peripheral vascular bed independently on renin and angiotensin converting enzyme.
Ischemic dog heart experiments suggested that kinin-tensin system plays a role in the formation of angiotensin II and kinin and participate in the progression of myocardial infarction after coronary artery occlusion. In the study of patients with arteriosclerosis obliterans, administration of trypsin- kallikrein inhibitor improved exercise tolerance.
Putatively new kinins, hydroxyproline^3- bradykinin and lysyl-bradykinin, .were discovered, and these kinins as well as bradykinin and lysys-bradykinin were suggested to regulate peripheral circulation by competitive inhibition of angiotensin converting enzyme in addition to those direct vasodilatory action.
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