Compensatory hypertrophy of the kidney in rats and rabbits after unilateral nephrectomy in early stages of postnatal ontogenesis

1970 ◽  
Vol 70 (1) ◽  
pp. 811-813
Author(s):  
M. S. Alimetova
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.


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.


1998 ◽  
Vol 126 (6) ◽  
pp. 1248-1250
Author(s):  
S. S. Timoshin ◽  
E. N. Sazonova ◽  
O. A. Lebed'ko ◽  
V. V. Kulaeva

2012 ◽  
Vol 302 (12) ◽  
pp. H2509-H2517 ◽  
Author(s):  
Kaylan M. Haizlip ◽  
Tepmanas Bupha-Intr ◽  
Brandon J. Biesiadecki ◽  
Paul M. L. Janssen

Numerous studies have aimed to elucidate markers for the onset of decompensatory hypertrophy and heart failure in vivo and in vitro. Alterations in the force-frequency relationship are commonly used as markers for heart failure with a negative staircase being a hallmark of decompensated cardiac function. Here we aim to determine the functional and molecular alterations in the very early stages of compensatory hypertrophy through analysis of the force-frequency relationship, using a novel isolated muscle culture system that allows assessment of force-frequency relationship during the development of hypertrophy. New Zealand white male rabbit trabeculae excised from the right ventricular free wall were utilized for all experiments. Briefly, muscles held at constant preload and contracting isometrically were stimulated to contract in culture for 24 h, and in a subset up to 48 h. We found that, upon an increase in the preload and maintaining the muscles in culture for up to 24 h, there was an increase in baseline force produced by isolated trabeculae over time. This suggests a gradual compensatory response to the impact of increased preload. Temporal analysis of the force-frequency response during this progression revealed a significant blunting (at 12 h) and then reversal of the positive staircase as culture time increased (at 24 h). Phosphorylation analysis revealed a significant decrease in desmin and troponin (Tn)I phosphorylation from 12 to 24 h in culture. These results show that even very early on in the compensatory hypertrophy state, the force-frequency relationship is already affected. This effect on force-frequency relationship may, in addition to protein expression changes, be partially attributed to the alterations in myofilament protein phosphorylation.


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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