1987 Fiscal Year Final Research Report Summary
Attempt for purification of proliferation promoting substance of arterial collateral endothelial cells after renal arthery stenosis in the rat.
Project/Area Number |
61570505
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Research Category |
Grant-in-Aid for General Scientific Research (C)
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Allocation Type | Single-year Grants |
Research Field |
Radiation science
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Research Institution | Fukui Medical School |
Principal Investigator |
ODOR teruo Fukui Medical School, Department of Radiology, 医学部, 助教授 (10115818)
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Co-Investigator(Kenkyū-buntansha) |
NAKATSUGAWA SHIGEKAZU Fukui Medical School, Department of Radiology, 医学部, 講師 (00180315)
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Project Period (FY) |
1986 – 1987
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Keywords | Renal artery stenosis / Hypertension / Collateral vessel formation / Endothelial hyperplasia / Captopril / 腫瘍血管 |
Research Abstract |
The rapidity with which collateral channels are recruited and the degree to which blood supply is maintained are major determinants of tissue survival after arterial occlusion. Despite their importance, however, the mechanisms responsible for collateral development remain poorly defined. Suggested mechanisms have involved an increased pressure gradient, pressure, the metabolic products of ischemic agents. In an attempt to substantiate the existence of humoral factors, the periureteric collateral blood supply to the kidney following renal artery occlusion was used as the model. Mameuvers were designed either to promote increased hypertension, or to prevent the hypertension with antihypertensive drugs. A surprising finding that the conventing enzyme inhibitor, captopril, increased the vascular proliferative response rather than reduced it represents the primary thrust of this study. The comparative study was first performed in the same ischemic renal model between hydralazin and captopril which were different in pharmacological effects. An unanticipated result was obtained that the absolute collateral blood flow around the renal hilum of the rat administered captopril for 6 weeks after stenosis surgery was significantly (p <0.05) decreased compared to control. (captopril, control, 0.18<plus-minus>0.049, 0.32<plus-minus>0.047 ml/kg/min, resectively) On the conntrary that the blood pressure of the former groop was lower than that of the latter. (Captopril, control; 139<plus-minus>8.33, 184<plus-minus>7.83 mmHg, respectively (to preve The most likely explanation for this result might be the time course of collateral formation after stenosis. It is will known that the renal collaterals are most actively formed during first week after stenosis surgery for which captopril may be effective in inducing endothelial hyperplastic reaction. It is under study that higher blood pressure system after then should play a more important role.
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Research Products
(11 results)