| First Author | Inokuchi S | Year | 1998 |
| Journal | Virchows Arch | Volume | 433 |
| Issue | 4 | Pages | 349-57 |
| PubMed ID | 9808437 | Mgi Jnum | J:50712 |
| Mgi Id | MGI:1309610 | Doi | 10.1007/s004280050259 |
| Citation | Inokuchi S, et al. (1998) Angiotensin II maintains the structure and function of glomerular mesangium via type 1a receptor. What we have learned from null mutant mice minus the angiotensin II type 1a receptor gene. Virchows Arch 433(4):349-57 |
| abstractText | The angiotensin II type la (AT1a) receptor is the major receptor effecting the multiple actions of angiotensin II on the cardiovascular system. It is expressed abundantly in the glomerular mesangial cells of the kidney. We investigated glomerular changes in null mutant mice minus the AT1a receptor gene to gain an understanding of the in vivo action of angiotensin II via AT1a on the mesangium, Morphological observations and morphometric analysis revealed that the glomerular volume was greatly increased owing to the expansion of the mesangial area, which contained fluid-filled spaces with a small amount of fibrillar components. The mesangial cells lost contact with each other and with the perimesangial area of the glomerular basement membrane (GBM), so that the glomerular capillary neck was greatly widened. These findings suggest a defect of the anchoring function of mesangial cells resulting from some abnormality in mesangial matrix formation. We conclude that angiotensin II has an important role in the structural and functional maintenance of the mesangium via the AT1a receptor, especially by reinforcing the connection between mesangial cells and GEM via the mesangial matrix. |
