Goya R G, Castelletto L, Sosa Y E
Centro de Estudios Endócrinos, Facultad de Ciencias Médicas, Universidad Nacional de La Plata, Argentina.
Lab Invest. 1991 Jan;64(1):29-34.
It is well known that pharmacologic administration of growth hormone (GH), prolactin (Prl) or adrenal steroids can induce nephrosclerotic lesions in rodents. In this study we correlated circulating levels of endogenous GH, Prl, and corticosterone with the degree of structural nephropathy in rats of different ages. Female young (3 to 4 months), old (25 months), and senescent (33 to 35 months) and male young (3 to 4 months) and old (24 to 26 months) Sprague-Dawley rats were used. Sequential blood samples were removed through intraatrial cannulas while the animals remained conscious and undisturbed. Plasma Prl showed a 3-fold increase in old compared with young males, while old and senescent females displayed a 13- and 64-fold increase, respectively, for Prl. Plasma GH decreased significantly in old compared with young males, while senescent females had elevated GH levels compared with their young and old counterparts. Plasma corticosterone showed an age-related decline in females but not in males. The kidneys from old males showed a marked degree of glomerular sclerosis and obliteration. The presence of tubular metaplasia of Bowman's capsule as well as deposits of iron in the tubular epithelium was common in old males but rare in old and senescent females. There was a strong correlation of plasma GH, but not Prl, with the severity of renal histopathology. Plasma corticosterone showed an inverse correlation with the severity of renal histopathology in old males and senescent females. These results are consistent with the hypothesis that GH contributes to nephrosclerosis of aging rats, whereas the role of corticosterone and Prl in the pathogenesis of these lesions remains unclear.
