抄録
Since the angiotensin-converting enzyme inhibitor has a potent suppressive effect upon the development of glomerular sclerosis, angiotensin II is believed to be involved in the disease progress. Angiotensin II causes glomerular hypertension, a proposed predominant factor leading to glomerular sclerosis, through more prominent contraction of the efferent than the afferent arterioles as well as through elevating systemic blood pressure. In vitro studies using cultured mesangial cells have revealed that angiotensin II also causes cell proliferation and matrix production, a hallmark of various glomerular diseases, as well as cell contraction which is important in the regulation of the glomerular filtration process. Furthermore, the contraction and proliferation of mesangial cells are biologically linked to each other and may play a synergistic role in the progression of glomerular sclerosis. The direct in vivo role of angiotensin II in physiological and pathophysiological regulation of mesangial cell functions should be further studied in future.
