Compensatory renal hypertrophy after nephrectomy in newborn rats]

The process of the kidney compensatory hypertrophy in young rats has been studied after nephrectomy on the 2nd day of life. The intact kidney was investigated by morphometrical and electron microscopical methods from the 1st day till the 3rd month after operation. The kidney compensatory hypertrophy in the early postnatal ontogenesis is accompanied by the acceleration of growth and differentiation of renal structures. The hypertrophy involves three successive steps: (1) functional tension of ultrastructures; (2) expressed hyperplasia and hypertrophy of cells; (3) structural-functional specialization. Among the cellular factors of the kidney compensatory growth at this age, the main role is played by the process of cell hyperplasia.     

Compensatory renal hypertrophy in rats. II. Possible regulatory role of renal inhibitory substance]

Clear supernatant from kidney homogenate injected to an uninephrectomized rat inhibits specifically the incorporation of tritiated thymidine by compensating kidney. This result agrees with the speculation of autoregulation of kidney growth.     

Compensatory hypertrophy of the adrenal glands following unilateral adrenalectomy in juvenile rats

Left-handed adrenalectomy in rats aged 1, 5, 10, 15, 20 and 30 days produces compensatory hypertrophy of the remaining gland. Hypertrophy of the right adrenal is unmarked and variable depending on the time elapsed after operation (1, 3, 5, 7, 14, 21 and 30 days). The index of hypertrophy as regards one right control adrenal does not exceed 133.6%, whereas that as regards both control adrenals 66.2%. Zona fasciculata reticularis plays the main role in the increase of the dimension and weight of the hypertrophied gland. The body weight of operated rats is lower as compared to control, the weight lag being inversely proportional to the animal's age at the moment of operation.     

Compensatory testicular hypertrophy in the lizard Anolis carolinensis

In reproductively responsive, male Anolis carolinensis undergoing artificially induced testicular recrudescence, unilateral orchidectomy of the left testis produced compensatory hypertrophy of the remaining testis. Testosterone inhibited this compensatory testicular hypertrophy on a weight basis, but did not reduce the rate of spermatogenic development. These results suggest that there is a mechanism of testosterone feedback in Anolis carolinensis that controls gonadotropin secretion during the recrudescent phase. In reproductively thermorefractory lizards, unilateral orchidectomy had no effect on the remaining testis. Administration of exogenous follicle-stimulating hormone to refractory animals increased testicular weight and stage of spermatogenic development. Sensitivity to gonadotropin, as well as failure of unilateral orchidectomy to produce compensatory hypertrophy in refractory male anoles, suggests that the control of the refractory period in A. carolinensis results from physiological mechanisms in the pituitary gland or brain rather than in the testis.     

Compensatory ovarian hypertrophy during alloxan diabetes and adrenoreceptor blockade

The sexual cycle ceases in rats with alloxan diabetes. Chronic administration of phentolamine promoted interruption of the sexual cycle while obsidan was conducive to its preservation in part of the animals. Most diabetic rats both given and not given adrenoblockers showed the complete absence of compensatory hypertrophy of the ovary (CHO). As shown by the analysis, the content of gonadotropins in the pituitary glands of diabetic rats was increased, with the response to chorionic gonadotropin being close to normal. It is suggested that the absence of CHO in most diabetic rats can be accounted for by the fact that after removal of one ovary the hypothalamohypophyseal system does not secrete gonadotropins in adequate amounts.