Compensatory hypertrophy of the kidney during various periods after unilateral nephrectomy in very young albino rats

1927 ◽  
Vol 36 (3) ◽  
pp. 221-237 ◽  
Author(s):  
C. M. Jackson ◽  
Margaret Shiels
1938 ◽  
Vol 67 (4) ◽  
pp. 515-519 ◽  
Author(s):  
Lois L. MacKay ◽  
T. Addis ◽  
Eaton M. MacKay

Compensatory hypertrophy of the kidney in albino rats is increased by an increase in the protein intake. The effect is greater in old rats than young rats. Successive increases in the protein intake are followed by a reduction in the increase in the degree of compensatory renal hypertrophy.


1932 ◽  
Vol 56 (2) ◽  
pp. 255-265 ◽  
Author(s):  
E. M. MacKay ◽  
L. L. MacKay ◽  
T. Addis

Compensatory hypertrophy of the kidney in albino rats becomes less as age advances. There is a rapid decrease from 5 days to 60 days of age and then a slow diminution throughout adult life.


2017 ◽  
Vol 32 (suppl_3) ◽  
pp. iii207-iii207
Author(s):  
Maria Paniagua-Sancho ◽  
Cristina Cuesta ◽  
Nuria Perretta-Tejedor ◽  
Nelida Eleno ◽  
Isabel Fuentes-Calvo ◽  
...  

1964 ◽  
Vol 46 (3) ◽  
pp. 352-360 ◽  
Author(s):  
Jan Jelínek ◽  
Hana Veselá ◽  
Blanka Valová

ABSTRACT Forty eight hours after unilateral nephrectomy, both in non-castrated and in castrated male mice the relative dry weight of the remaining kidney increased significantly. This compensatory hypertrophy was significantly stimulated as early as 96 hours after operation by the treatment with 19-nortestosterone phenylpropionate (= NPP) at the time of operation. The percentual increase of the kidney weight was approximately the same in non-castrated as in castrated mice. The absolute initial values as well as the resulting values 96 hours after operation were higher in non-castrated male mice than in castrated animals. The number of cells and the DNA concentration per g tissue decreased during the period of non-stimulated compensatory hypertrophy in both groups of animals. NPP caused a still further decrease. The concentration of DNA per cell did not change. Following non-stimulated compensatory hypertrophy, there was no change in the RNA concentration per g tissue or per cell in castrated mice. In non-castrated mice the concentration increased. NPP caused approximately the same percentual increase of RNA concentration in non-castrated as in castrated animals during the period of compensatory hypertrophy. The difference between both groups of mice in the RNA concentration in the remaining kidney following stimulation of the compensatory hypertrophy by NPP was statistically significant.


1957 ◽  
Vol 105 (6) ◽  
pp. 501-508 ◽  
Author(s):  
Phyllis M. Hartroft

Hypertension in rats produced by constriction of one renal artery was associated with degranulation of juxtaglomerular cells in the contralateral, undamped, kidney. These findings are consistent with those of other investigators. Furthermore, the degree of granulation (JGI) in the unclamped kidney was inversely correlated with the level of blood pressure (r = –0.7). Degranulation of JG cells also occurred in rats made hypertensive by application of a "figure-of-eight" ligature to one kidney and removal of the other one, except when the interference in blood supply was so severe that scarring resulted. In these damaged areas, granules persisted or increased in number even though they were decreased in adjacent relatively normal areas. Occlusion of one ureter in rats produced severe hydronephrosis in the homolateral kidney and an elevation in blood pressure. Juxtaglomerular cell granules persisted in the hydronephrotic kidney but were decreased in the contralateral one. This finding confirmed the results of the above experiments. Unilateral nephrectomy in comparable rats had no effect on the degree of granulation of JG cells in the remaining kidney or on the level of blood pressure under the conditions of these experiments. The possibility that degranulation of JG cells in the contralateral kidney in the rats described above was due to compensatory hypertrophy was thereby excluded. An elevation in blood pressure was therefore implicated as an important factor in causing degranulation of juxtaglomerular cells.


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