1992 Fiscal Year Final Research Report Summary
Angiotensin II and Kinin formation by vascular endothelial and smooth muscle cells
| Project/Area Number |
03670473
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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 | Fukuoka University |
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Principal Investigator |
IDEISHI Munehito Fukuoka University School of Medicine, Lecturer, 医学部, 講師 (20131807)
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| Project Period (FY) |
1991 – 1992
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| Keywords | Angiotensin / bradykinin / endothelial cell / smooth muscle cell / chymostatin |
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| Research Abstract |
Angiotensin II or kinin forming activities in two types of cell lines (cow pulmonary endothelial cells(CPAE) and rat aortic smooth muscle cells(A-10)) and in cells from primary cultures of porcine aortic endothelial(PAEC) and smooth muscle cells(PASMC) were investigated.
Methods ; Cells were plated at a concentration of 50,000/cm^2 in 6-well plates. At confluence, cells were incubated in serum-free medium with authentic substrates(angiotensin(ANG) I, tridecapeptide renin substrate(13-RS), and tetradecapeptide renin substrate(14-RS). After incubation for I hr, reactions were terminated by the addition of IICI, the mediun was extracted by reverse phase cartridges, and processed for HPLC. Angiotensin II or bradykinin in appropriate fractions were measured by specific radioimmunoassay. Effects of enzyme inhibitors, captopril(CAPT), chymostatin (CIIYM) and aprotinin were also determined.
Results ; Both CPAE and PAEC converted ANG I to ANG II efficiently, and those activities were inhibited al
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most completely by CAPT but not by CIIYM. CPAE formed AAG II from 13RS in the presence of CAPT, and this activity was inhibited partially by CIIYM. A-10 showed modest activity of converting ANG I to ANG II, which was inhibited by CAPT. ANG II formation from 13RS by A-10 was more efficient than by CPAE. This was also inhibited by CIIYM partially. Conversion of ANG I to II by PASMC was almost equal with that of PAEC. Both PASMC and PAEC formed ANG II from porcine specific renin substrate(14RS) in the presence of CAPT. In contrast to the case of CPAE or A-10, the non-ACE dependent ANG II formation by PAEC or PASMC were relatively insensitive to CIIYM. PASMC formed bradykinin form KNG, and the activity was sensitive to aprotinin.
Conclusion ; Vascular endothelial and smooth muscle cells were shown to form ANG II by two, i.e. ACE-dependent and independent pathways. The contribution of each pathway to form ANG II was different in each cell type and species. The presence of Aprotinin-sensitive, Kallikrein-like enzyme in vascular SMC was suggested. Less
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Research Products
(2 results)
