scholarly journals Conservation of ribosomal RNA during compensatory renal hypertrophy. A major mechanism in RNA accretion.

1976 ◽  
Vol 69 (3) ◽  
pp. 548-556 ◽  
Author(s):  
W T Melvin ◽  
A Kumar ◽  
R A Malt
Keyword(s):  
Ribosomal Rna ◽  
Cultured Cells ◽  
Compensatory Hypertrophy ◽  
Mouse Kidney ◽  
Average Increase ◽  
Renal Hypertrophy ◽  
Major Mechanism ◽  
Compensatory Renal Hypertrophy

After removal of one mouse kidney, compensatory hypertrophy in the remaining kidney is marked in 2 days by a 20% average increase in ribosomal RNA (rRNA) per cell. Both 28S and 18S RNA are conserved during the initial stages of compensatory renal hypertrophy to an extent sufficient to account for the rest of the observed accumulation of rRNA. Like some cultured cells, the kidney conserves rRNA during physiological growth.

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.

Compensatory renal hypertrophy. I. Evidence for a factor of renal origin inhibiting DNA synthesis

1977 ◽  
Vol 55 (4) ◽  
pp. 839-847 ◽  
Author(s):  
J. Martel-Pelletier ◽  
M. Bergeron
Keyword(s):  
Molecular Weight ◽  
Dna Synthesis ◽  
Specific Inhibitor ◽  
Inhibitory Effect ◽  
Compensatory Hypertrophy ◽  
Partial Purification ◽  
Dna Uptake ◽  
Renal Hypertrophy ◽  
Compensatory Renal Hypertrophy

This study describes a method for the measurement and partial purification of a factor seemingly involved in the regulation of the renal mass.After homogenization at 4 °C, rabbit kidneys were centrifuged for 100 min at 105 000 g. The resulting supernatant (S-105) was lyophilized and tested on kidney slices obtained from rats mononephrectomized 48 h previously. We have developed a method based on the inhibition of DNA synthesis to measure the activity of the S-105. Slices of renal cortex, undergoing compensatory hypertrophy, were incubated in vitro in Hanks' medium at 37 °C, pH 7.4, in an O2–CO2 atmosphere in the presence of 0.144 μg (20 μCi (1 Ci = 37 GBq)) [3H]thymidine.An inhibition of DNA uptake of [3H]thymidine was noted in the presence of S-105. When other media (Hanks', sucrose, water) were used to extract S-105, the same type of inhibition was noted even though the sucrose buffer seemed ideal for the preservation of the inhibitory factor. The inhibitory effect was still observed after dialysis of S-105 against membranes permitting exclusion of molecules with molecular weight smaller than about 4000 (such as electrolytes and tissue thymidine). This inhibition seems to be specific, since other tissues such as liver in regeneration and rat intestine were not influenced by the dialyzed renal S-105. The dialyzable fraction did contain some inhibitors, but they were not specific for the kidney since they also acted on the liver and the jejunum.Our results suggest the existence, in the normal nephron, of a specific inhibitor of thymidine incorporation into DNA of kidneys undergoing a compensatory hypertrophy. This renal factor has a molecular weight of over 5000.

scholarly journals Ribonucleic acid labelling and nucleotide pools during compensatory renal hypertrophy

1974 ◽  
Vol 144 (3) ◽  
pp. 447-453 ◽  
Author(s):  
J M Hill ◽  
G Ab ◽  
R A Malt
Keyword(s):  
Rna Synthesis ◽  
Single Injection ◽  
Specific Radioactivity ◽  
Compensatory Hypertrophy ◽  
Rrna Synthesis ◽  
Renal Hypertrophy ◽  
Rna Content ◽  
Compensatory Renal Hypertrophy ◽  
Precursor Rna ◽  
Ribosomal Precursor

During the first 48h of compensatory renal hypertrophy induced by unilateral nephrectomy, RNA content per cell increased by 20–40%. During this period, rates of RNA synthesis derived from the rates of labelling of UTP and RNA after a single injection of [5-3H]uridine showed no change in the rate of RNA synthesis (3.1nmol of UTP incorporated into RNA/min per mg of RNA). ATP and ADP pools were not changed. The rate of RNA synthesis was considerably in excess of the increment of total RNA appearing in the kidneys. With [5-3H]uridine as label, only continuous infusion for 24h could produce an increase (60%) in the specific radioactivity of renal rRNA in mice with contralateral nephrectomies. With a single injection of [methyl-3H]methionine used to identify methyl groups inserted into newly synthesized rRNA, the specific radioactivity of this rRNA was unchanged 5h after contralateral nephrectomy, increased by 60% at 9–48h, and returned to normal values at 120h. Most RNA synthesized in both nephrectomized and sham-nephrectomized mice has a short half-life. Since total cellular RNA content increases in compensatory hypertrophy despite unchanged rates of rRNA synthesis, the accretion of RNA might involve conservation of ribosomal precursor RNA or a change in rate of degradation of mature rRNA.

Noncoordinate regulation of cytoplasmic RNA in compensatory renal hypertrophy

1979 ◽  
Vol 237 (5) ◽  
pp. R360-R365
Author(s):  
A. J. Ouellette ◽  
R. A. Malt
Keyword(s):  
Cell Growth ◽  
Orotic Acid ◽  
Control Mechanism ◽  
Mouse Kidney ◽  
Renal Hypertrophy ◽  
Polyadenylated Rna ◽  
Cytoplasmic Rna ◽  
Compensatory Renal Hypertrophy ◽  
Mrna Half Life

To examine the regulatory role of mRNA in compensatory renal hypertrophy, the accumulation and decay of [3H]orotic acid in poly(A)-containing mRNA in mouse kidney was analyzed after unilateral nephrectomy during the period of maximal rRNA accretion. The distribution of radioactivity between newly synthesized poly(A)-containing and poly(A)-lacing polysomal RNA was altered, but no differences in mRNA half-life were observed in growth compared with effects of sham nephrectomy. Radioactivity in polysomal polyadenylated RNA was diminished by approximately 25% during growth where mice were labeled after nephrectomy, but if mice were labeled 18 h before operation, no difference was noted. Thus, accumulation of newly synthesized poly(A)-containing mRNA relative to RNAs that lack poly(A) is changed early in the course of renal hypertrophy. This noncoordinate regulation may represent a control mechanism effective early in induced cell growth involving mRNAs that lack poly(A).

Differential labeling with orotic acid and uridine in compensatroy renal hypertrophy

1975 ◽  
Vol 229 (4) ◽  
pp. 952-954 ◽  
Author(s):  
JS Ross ◽  
D Malamud ◽  
JA Caulfield ◽  
RA Malt
Keyword(s):  
Orotic Acid ◽  
Compensatory Hypertrophy ◽  
Mouse Kidney ◽  
Proximal Tubules ◽  
Renal Hypertrophy ◽  
Tubular Cells ◽  
Biologic Activity ◽  
Distal Tubules ◽  
Labeled Rna

Using [5-3H]orotic acid and [5-3H]uridine as precursors, we compared the efficiency of labeling and the localization of labeled RNA during compensatory hypertrophy of the mouse kidney. [5-3H]orotic acid in tubules labeled RNA 15 times more intensely that [5-3H]uridine, presumably because of greater incorporation of orotic acid into tubular cells. Of the orotic acid label, 97% was in tubular cells, mostly in the proximal tubules. Only about 80% of the uridine label was in the tubules; the ratio in proximal tubules compared with that in distal tubules was 2:1. No changes in distribution within the nephron were produced during compensatory hypertrophy. [5-3H]uridine should be used as the precursor of generalized labeling is desired, but [5-3H5orotic acid is the better precursor of RNA for many studies of compensatory hypertrophy since it is more efficient and concentrates in the segments of greatest biologic activity.

scholarly journals Synthesis and conservation of ribosomal proteins during compensatory renal hypertrophy

1980 ◽  
Vol 188 (1) ◽  
pp. 229-235 ◽  
Author(s):  
W T Melvin ◽  
A Kumar ◽  
R A Malt
Keyword(s):  
Protein Synthesis ◽  
Total Protein ◽  
Ribosomal Proteins ◽  
Mouse Kidney ◽  
Renal Hypertrophy ◽  
Ribosomal Subunits ◽  
Synthetic Rate ◽  
Compensatory Renal Hypertrophy ◽  
Major Increase ◽  
Ribosomal Protein Synthesis

The rate of synthesis of ribosomal proteins was investigated as an index of the rate of production of ribosomes in mouse kidney during the first few days after contralateral nephrectomy. Compensatory renal hypertrophy was not associated with a major increase in the synthetic rate of ribosomal proteins and rRNA. Instead, the ratio of the rate of ribosomal-protein synthesis to that of total protein synthesis remained nearly constant. The conformation of glutaraldehyde-fixed ribosomes and ribosomal subunits was unchanged. During the early stages of compensatory renal hypertrophy the accretion of rRNA is due largely to conservation of ribosomes that would otherwise have been degraded.

Relative Resistance to the Hypertensive Effects of Desoxycorticosterone During Active Phase of Renal Compensatory Hypertrophy

1958 ◽  
Vol 194 (2) ◽  
pp. 236-240 ◽  
Author(s):  
C. E. Hall ◽  
O. Hall
Keyword(s):  
Active Phase ◽  
Hormone Treatment ◽  
Compensatory Hypertrophy ◽  
Renal Tubules ◽  
Sodium Retention ◽  
Relative Resistance ◽  
Renal Hypertrophy ◽  
Kidney Size ◽  
Compensatory Renal Hypertrophy ◽  
Desoxycorticosterone Acetate

An attempt was made to ascertain the circumstances under which unilateral nephrectomy maximally sensitized rats to hypertensive cardiovascular disease induced by desoxycorticosterone acetate in the presence of augmented NACl intake. The experiments showed that animals in which hormone treatment was delayed until 2 weeks after uninephrectomy were much more sensitive than animals in which hormone treatment was begun on the day of kidney removal. This was indicated by earlier onset and greater severity of hypertension; by a larger percentage of animals in such groups being affected, and by a greater incidence and severity of cardiovascular lesions in the former as compared with the latter. The much greater kidney size of the former clearly makes it difficult to ascribe the greater sensitivity to a reduction in renal mass as such. It is thought that during active compensatory renal hypertrophy the renal tubules are probably less responsive to the action of the hormone and therefore less prone to develop sodium retention and hence hypertension.

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.

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