| First Author | Sigmund CD | Year | 1991 |
| Journal | Am J Physiol | Volume | 260 |
| Issue | 2 Pt 2 | Pages | F249-57 |
| PubMed ID | 1996675 | Mgi Jnum | J:79925 |
| Mgi Id | MGI:2389584 | Doi | 10.1152/ajprenal.1991.260.2.F249 |
| Citation | Sigmund CD, et al. (1991) Pathophysiology of vascular smooth muscle in renin promoter-T-antigen transgenic mice. Am J Physiol 260(2 Pt 2):F249-57 |
| abstractText | The pathophysiological consequence of targeted production of SV-40 T-antigen to renin-expressing cells in the kidney of transgenic mice is reported. A histopathologic analysis of the kidney from adult transgenic mice (12-16 wk old) revealed the presence of severe vascular lesions manifested by marked atypical hyperplasia of vascular smooth muscle. The levels of plasma renin, kidney renin, and kidney renin mRNA were examined in 6- and 9-wk-old transgenic mice and were found to be significantly lower than their age-matched non-transgenic littermates and were nonresponsive to captopril treatment. However, there was no significant difference in conscious mean arterial pressure between transgenic and non-transgenic mice. The levels of renal renin mRNA in transgenics and nontransgenic littermates were compared throughout ontogeny and were found to be equal in newborns, elevated 3- to 5-fold in 1-wk-old transgenics, and yet decreased 10-fold by 6 wk of age in transgenic mice. Expression of the transgene in the kidney exhibited the proper developmental pattern and was properly restricted to juxtaglomerular cells in neonatal mice. Nevertheless, in adult mice, T-antigen-containing cells were found throughout the entire renal arterial tree. The observed ability of renal vascular cells to be recruited to express both renin and T-antigen suggests a mechanism that can explain the development of the renal pathology in these mice. |
