| Budget Amount *help |
¥2,500,000 (Direct Cost: ¥2,500,000)
Fiscal Year 1992: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1991: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1990: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Research Abstract |
The intraglomerular pressure has been suggested to play an important role in development of glomerulusclerosis. The systemic pressure and pre- and post-glomerular arterioles determine the glomerular pressure and thus functional abnormalities in renal arterioles might leads to glomerular damage. In the present study, we investigated changes in the renal arteriolar diameters in various experimental models and tried to clarify the relationship between arterioles and glomerular damage.
First, we demonstrated that the changes in arteriolar diameters were parallel to the changes in renal function and that changes in arteriolar diameters during the procedure of casting was not significant. These findings show that we can use microvascular casts in the present study. In the spontaneously hypertensive rats, streptozotocin diabetic rats, subtotally nephrectomized rats and anti-glomerular basement membrane nephritis rats, we showed that the renal arteriolar diameters and the systemic blood pressur
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e were important factor for the development of glomerulusclerosis and arteriolar dysfunction augmented glomerular damage. However, in the intervention study with antihypertensive agents, non-hemodynamic factors were suggested to play an important role in development of glomerulusclerosis in addition to hemodynamic factors. Accordingly, integrated studies on the mechanisms of development of glomerulusclerosis are necessary in the future.
In the present study, we developed techniques to investigate renal arterioles in vivo under the microscope using hydronephrotic rats. Using this model, we revealed that manidipine hydrochloride dilated the efferent arterioles as well as the afferent arterioles, which is consistent with our previous micropuncture study. In spontaneously hypertensive rats, we also investigated arteriolar responses to other calcium channel blockers, angiotensin converting enzyme inhibitors, beta-blockers et al. Now we are going to investigate arteriolar dysfunction in various experimental model using this model. Less
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