Intraglomerular expression of alpha-smooth muscle actin in aging mice.

To determine whether chronic treatment with enalapril initiated early in life prevents glomerular injury secondary to normal aging, CF1 mice received enalapril (20 mg/L, n = 10) or nifedipine (40 mg/L, n = 10) in their drinking water from the time of weaning to 12 months of life. Control mice (n = 10) received tap water ad libitum. Immunocytochemical detection of renin confirmed that angiotensin-converting enzyme inhibition resulted in recruitment of renin-containing cells along the preglomerular vessels. Morphometric analysis of glomeruli included assessment of glomerular diameter and the percentage of mesangial area per glomerulus. Glomerular diameter and mesangial area were higher in control mice (99.7 +/- 0.5 microns, 12.7 +/- 0.3%) than in enalapril-treated mice (88 +/- 0.8 microns, 8.6 +/- 0.6%) (P < .05). Glomerular diameter and mesangial area in the nifedipine-treated group (99.1 +/- 0.9 microns, 12.4 +/- 0.9%) were not different from control mice. These results demonstrate that angiotensin-converting enzyme inhibition prevents the glomerular enlargement and mesangial expansion observed during natural aging. In addition, control glomeruli expressed alpha-smooth muscle actin in a mesangial distribution. This effect was prevented by enalapril treatment but not by nifedipine. We conclude that long-term treatment with enalapril from early life prevents the early changes associated with glomerular injury and expression of alpha-smooth muscle actin in the glomerulus. alpha-Smooth muscle actin may participate in and serve as an early marker of the glomerular injury during the normal aging process.