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 t heir drinking water from the time of weaning to 12 months of life. Con trol mice (n=10) received tap water ad libitum. Immunocytochemical det ection of renin confirmed that angiotensin-converting enzyme inhibitio n resulted in recruitment of renin-containing cells along the preglome rular vessels. Morphometric analysis of glomeruli included assessment of glomerular diameter and the percentage of mesangial area per glomer ulus. Glomerular diameter and mesangial area were higher in control mi ce (99.7+/-0.5 mu m, 12.7+/-0.3%) than in enalapril-treated mice (88+/ -0.8 mu m, 8.6+/-0.6%) (P<.05). Glomerular diameter and mesangial area in the nifedipine-treated group (99.1+/-0.9 mu m, 12.4+/-0.9%) were n ot different from control mice. These results demonstrate that angiote nsin-converting enzyme inhibition prevents the glomerular enlargement and mesangial expansion observed during natural aging. In addition, co ntrol glomeruli expressed alpha-smooth muscle actin in a mesangial dis tribution. 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 injur y and expression of alpha-smooth muscle actin in the glomerulus. alpha -Smooth muscle actin may participate in and serve as an early marker o f the glomerular injury during the normal aging process.