Nephrol Dial Transplant (2003) 18: 1966-1969
© 2003 European Renal Association-European Dialysis and Transplant Association
Editorial Comment
The mechanisms underlying altered vascular resistance of glomerular afferent and efferent arterioles in diabetic nephropathy
Division of Nephrology, Endocrinology and Vascular Medicine, Tohoku University School of Medicine, Sendai, Japan
Correspondence and offprint requests to: Shuji Arima, MD, Division of Nephrology, Endocrinology and Vascular Medicine, Tohoku University School of Medicine, 1–1 Seiryo-cho, Aoba-ku, Sendai 980-8574, Japan. Email: shuarima@mail.cc.tohoku.ac.jp
Keywords: atrial natriuretic peptide; calcium and potassium channel; insulin; myogenic response; renin–angiotensin system; tubuloglomerular feedback
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Introduction
In diabetes and various renal diseases, glomerular capillary pressure (PGC) is elevated due to either decreased afferent arteriolar resistance or increased efferent arteriolar resistance, or both [1,2]. Regardless of initial insults, however, glomerular hypertension causes endothelial, mesangial and podocyte injuries, which ultimately result in glomerulosclerosis [3]. This decreases the number of functioning nephrons and further elevates PGC, thereby resulting in a vicious cycle. Thus, such alterations in glomerular haemodynamics critically contribute to the pathophysiology of diabetic nephropathy; particularly, it greatly influences the mode of progression of glomerular damage [2]. It is therefore important to understand mechanisms that alter glomerular haemodynamics in diabetes mellitus. This article reviews the mechanisms underlying altered vascular resistance of afferent or efferent arterioles in diabetic nephropathy.
Calcium and potassium channels
Afferent arteriolar dilation observed in early stage diabetes is associated with its diminished responses to a variety of vasoconstrictor
Tubuloglomerular feedback
Myogenic response
Insulin
Atrial natriuretic peptide
Renin–angiotensin system
Other factors and concluding remarks
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