Renal arterioles in development of glomerular sclerosis.

肾小球内压在肾小球硬化的发生发展中起重要作用。体循环压力和肾小球前、后小动脉决定肾小球压力，因此肾小动脉功能异常可能导致肾小球损害。在本研究中，我们研究了各种实验模型中肾小动脉直径的变化，并试图阐明小动脉与肾小球损伤之间的关系。首先，我们证明了小动脉直径的变化与肾功能的变化是平行的，并且在铸造过程中小动脉直径的变化不明显。这些结果表明，我们可以在本研究中使用微血管铸型。在自发性高血压大鼠、链脲佐菌素糖尿病大鼠、肾次全切除大鼠和抗肾小球基底膜肾炎大鼠中，我们发现肾小动脉直径和全身血压均显著高于正常对照组， ...更多信息 e是肾小球硬化发展的重要因素，小动脉功能障碍加重肾小球损害。然而，在抗高血压药物的干预研究中，除了血流动力学因素外，非血流动力学因素在肾小球硬化的发展中起重要作用。因此，对肾小球硬化发生机制的综合研究是必要的。在本研究中，我们开发了在活体显微镜下研究肾积水大鼠肾小动脉的技术。使用这个模型，我们发现盐酸马尼地平扩张传出小动脉以及传入小动脉，这与我们以前的微穿刺研究是一致的。在自发性高血压大鼠中，我们也研究了小动脉对其他钙通道阻滞剂、血管紧张素转换酶抑制剂、β受体阻滞剂等的反应。现在我们将使用该模型在各种实验模型中研究小动脉功能障碍。少

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 … More 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