| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1989: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1988: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Research Abstract |
Glomerular mesangial cells are known to have receptors specific to angiotensin II, to entract in response to angiotensin II and, thus, to contribute to the regulation of glomerular filtration rates. Since it has been recently reported that mesangial cells are able to produce renin, dysfunction of mesangial cells may impair the activity of intrarenal renin-angiotensin system and, thus, produce intrarenal hemodynamic alterations characteristic to diabetes. In order to evaluate the association of the changes in intrarenal renin- angiotensin system with hemodynamic alterations in diabetes, messenger RNA levels of renin and angioten- sinogen and angiotensin converting enzyme (ACE) activity in cultured mesangial cells and in kidneys of diabetic rats were examined.
Neither messenger RNA of renin or angiotensinogen nor ACE activity was detected in glomerular mesangial cells cultured under various conditions, indicating that mesangial cells could function only as an effector of renin-angiotensin system. Messenger RNA levels of renin and angiotensinogen in kidneys of diabetic rats were not different from those in kidneys of control rats. In contrast to these results, ACE activity in kidneys (in both outer cortex and inner cortex plus outer medulla) of diabetic rats was significantly reduced compared with that of control rats.
These results indicate that the main change in intrarenal renin-angiotensin system in diabetes is decrease in ACE activity, which could result in decrease in generation of intrarenal angiotensin II, leading to vasodilatation of arterioles characteristic to diabetes.
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