Comparison of compensatory hypertrophy of the kidney after unilateral nephrectomy on adult and senile rats

1976 ◽  
Vol 82 (5) ◽  
pp. 1744-1748
Author(s):  
V. F. Sidorova ◽  
V. D. Gorbunova
Keyword(s):  
Compensatory Hypertrophy ◽  
Unilateral Nephrectomy

scholarly journals THE DEGREE OF COMPENSATORY RENAL HYPERTROPHY FOLLOWING UNILATERAL NEPHRECTOMY

1938 ◽  
Vol 67 (4) ◽  
pp. 515-519 ◽  
Author(s):  
Lois L. MacKay ◽  
T. Addis ◽  
Eaton M. MacKay
Keyword(s):  
Protein Intake ◽  
Compensatory Hypertrophy ◽  
Unilateral Nephrectomy ◽  
Albino Rats ◽  
Renal Hypertrophy ◽  
Young Rats ◽  
Compensatory Renal Hypertrophy ◽  
Old Rats

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.

scholarly journals SP299ROLE OF CARDIOTROPHIN-1 IN THE DEVELOPMENT OF RENAL COMPENSATORY HYPERTROPHY AFTER UNILATERAL NEPHRECTOMY IN MICE

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

THE EFFECT OF NORTESTOSTERONE PHENYLPROPIONATE ON COMPENSATORY HYPERTROPHY OF THE REMAINING KIDNEY AFTER UNILATERAL NEPHRECTOMY

1964 ◽  
Vol 46 (3) ◽  
pp. 352-360 ◽  
Author(s):  
Jan Jelínek ◽  
Hana Veselá ◽  
Blanka Valová
Keyword(s):  
Dry Weight ◽  
Compensatory Hypertrophy ◽  
Unilateral Nephrectomy ◽  
Male Mice ◽  
Kidney Weight ◽  
The Difference ◽  
Time Of Operation ◽  
Rna Concentration ◽  
Number Of Cells ◽  
Stimulation Of

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.

scholarly journals STUDIES ON RENAL JUXTAGLOMERULAR CELLS

1957 ◽  
Vol 105 (6) ◽  
pp. 501-508 ◽  
Author(s):  
Phyllis M. Hartroft
Keyword(s):  
Blood Pressure ◽  
Renal Artery ◽  
Blood Supply ◽  
Compensatory Hypertrophy ◽  
The Other ◽  
Unilateral Nephrectomy ◽  
Juxtaglomerular Cells ◽  
Contralateral Kidney ◽  
Juxtaglomerular Cell ◽  
Hydronephrotic Kidney

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.

Endothelial dysfunction promotes the transition from compensatory renal hypertrophy to kidney injury after unilateral nephrectomy in mice

2012 ◽  
Vol 302 (11) ◽  
pp. F1402-F1408 ◽  
Author(s):  
Hajime Nagasu ◽  
Minoru Satoh ◽  
Kengo Kidokoro ◽  
Yuko Nishi ◽  
Keith M. Channon ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Soluble Guanylate Cyclase ◽  
Kidney Injury ◽  
Compensatory Hypertrophy ◽  
Initiation Factor ◽  
Unilateral Nephrectomy ◽  
Wild Type ◽  
Renal Hypertrophy ◽  
No Donor ◽  
Compensatory Renal Hypertrophy

Loss of functional nephrons associated with chronic kidney disease induces glomerular hyperfiltration and compensatory renal hypertrophy. We hypothesized that the endothelial nitric oxide synthase (eNOS) [soluble guanylate cyclase (sGC)] protein kinase G (PKG) pathway plays an important role in compensatory renal hypertrophy after unilateral nephrectomy. Analysis of mice subjected to unilateral nephrectomy showed increases in kidney weight-to-body weight and total protein-to-DNA ratios in wild-type but not eNOS knockout (eNOSKO) mice. Serum creatinine and blood urea nitrogen increased after nephrectomy in eNOSKO but not in wild-type mice. Furthermore, Bay 41–2272, an sGC stimulator, induced compensatory renal hypertrophy in eNOSKO mice and rescued renal function. The NO donor S-nitrosoglutathione (GSNO) and Bay 41–2272 stimulated PKG activity and induced phosphorylation of Akt protein in human proximal tubular cells. GSNO also induced phosphorylation of eukaryotic initiation factor 4E-binding protein and ribosomal protein S6. Our results highlight the importance of the eNOS-NO-PKG pathway in compensatory renal hypertrophy and suggest that reduced eNOS-NO bioavailability due to endothelial dysfunction is the underlying mechanism of failure of compensatory hypertrophy and acceleration of progressive renal dysfunction.

scholarly journals THE DEGREE OF COMPENSATORY RENAL HYPERTROPHY FOLLOWING UNILATERAL NEPHRECTOMY

1932 ◽  
Vol 56 (2) ◽  
pp. 255-265 ◽  
Author(s):  
E. M. MacKay ◽  
L. L. MacKay ◽  
T. Addis
Keyword(s):  
Adult Life ◽  
Compensatory Hypertrophy ◽  
Rapid Decrease ◽  
Unilateral Nephrectomy ◽  
Albino Rats ◽  
Renal Hypertrophy ◽  
Compensatory Renal Hypertrophy

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.

A translational model of chronic heart failure in rats

2018 ◽  
pp. 136-148
Author(s):  
С.А. Крыжановский ◽  
И.Б. Цорин ◽  
Е.О. Ионова ◽  
В.Н. Столярук ◽  
М.Б. Вититнова ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Chronic Heart Failure ◽  
Left Ventricular ◽  
Compensatory Hypertrophy ◽  
Experimental Myocardial Infarction ◽  
Left Ventricular Ejection ◽  
Translational Model ◽  
Innovative Drug ◽  
Ventricular Ejection Fraction

Цель исследования - разработка трансляционной модели хронической сердечной недостаточности (ХСН) у крыс, позволяющей, с одной стороны, изучить тонкие механизмы, лежащие в основе данной патологии, а с другой стороны, выявить новые биомишени для поиска и изучения механизма действия инновационных лекарственных средств. Методика. Использован комплекс эхокардиографических, морфологических, биохимических и молекулярно-биологических исследований, позволяющий оценивать и дифференцировать этапы формирования ХСН. Результаты. Динамические эхокардиографические исследования показали, что ХСН формируется через 90 дней после воспроизведения переднего трансмурального инфаркта миокарда. К этому времени у животных основной группы отмечается статистически значимое по сравнению со 2-ми сут. после воспроизведения экспериментального инфаркта миокарда снижение ФВ левого желудочка сердца (соответственно 55,9 ± 1,4 и 63,9 ± 1,6%, р = 0,0008). Снижение насосной функции сердца (на 13% по сравнению со 2-ми сут. после операции и на ~40% по сравнению с интактными животными) сопровождается увеличением КСР и КДР (соответственно с 2,49 ± 0,08 до 3,91 ± 0,17 мм, р = 0,0002, и с 3,56 ± 0,11 до 5,20 ± 0,19 мм, р = 0,0001), то есть к этому сроку развивается сердечная недостаточность. Результаты эхокардиографических исследований подтверждены данными морфометрии миокарда, продемонстрировавшими дилатацию правого и левого желудочков сердца. Параллельно проведенные гистологические исследования свидетельствуют о наличии патогномоничных для данной патологии изменений миокарда (постинфарктный кардиосклероз, компенсаторная гипертрофия кардиомиоцитов, очаги исчезновения поперечной исчерченности мышечных волокон и т.д.) и признаков венозного застоя в легких и печени. Биохимические исследования выявили значимое увеличение концентрации в плазме крови биохимического маркера ХСН - мозгового натрийуретического пептида. Данные молекулярно-биологических исследований позволяют говорить о наличии гиперактивности ренин-ангиотензин-альдостероновой и симпатоадреналовой систем, играющих ключевую роль в патогенезе ХСН. Заключение. Разработана трансляционная модель ХСН у крыс, воспроизводящая основные клинико-диагностические критерии этого заболевания. Показано наличие корреляции между морфометрическими, гистологическими, биохимическими и молекулярными маркерами прогрессирующей ХСН и эхокардиографическими диагностическими признаками, что позволяет использовать неинвазивный метод эхокардиографии, характеризующий состояние внутрисердечной гемодинамики, в качестве основного критерия оценки наличия/отсутствия данной патологии. Aim. Development of a translational model for chronic heart failure (CHF) in rats to identify new biotargets for finding and studying mechanisms of innovative drug effect in this disease. Methods. A set of echocardiographic, morphological, biochemical, and molecular methods was used to evaluate and differentiate stages of CHF development. Results. Dynamic echocardiographic studies showed that CHF developed in 90 days after anterior transmural myocardial infarction. By that time, left ventricular ejection fraction was significantly decreased in animals of the main group compared with rats studied on day 2 after experimental myocardial infarction (55.9 ± 1.4% vs . 63.9 ± 1.6%, respectively, p<0.0008). The decrease in heart’s pumping function (by 13% compared with day 2 after infarction and by approximately 40% compared to intact animals) was associated with increased ESD and EDD (from 2.49 ± 0.08 to 3.91 ± 0.17 mm, p = 0.0002, and from 3.56 ± 0.11 to 5.20 ± 0.19 mm, respectively, p = 0.0001); therefore, heart failure developed by that time. The results of echocardiographic studies were confirmed by myocardial morphometry, which demonstrated dilatation of both right and left ventricles. Paralleled histological studies indicated presence of the changes pathognomonic for this myocardial pathology (postinfarction cardiosclerosis, compensatory hypertrophy of cardiomyocytes, foci of disappeared transverse striation of muscle fibers, etc.) and signs of venous congestion in lungs and liver. Biochemical studies demonstrated a significant increase in plasma concentration of brain natriuretic peptide, a biochemical marker of CHF. Results of molecular studies suggested hyperactivity of the renin-angiotensin-aldosterone and sympathoadrenal systems, which play a key role in the pathogenesis of CHF. Conclusions. A translational model of CHF in rats was developed, which reproduced major clinical and diagnostic criteria for this disease. Morphometric, histological, biochemical, and molecular markers for progressive CHF were correlated with echocardiographic diagnostic signs, which allows using this echocardiographic, noninvasive method characterizing the intracardiac hemodynamics as a major criterion for the presence / absence of this pathology.

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