An Inhibition of Urinary Albumin Excretion by Protease Inhibitor in Streptozotocin-Diabetic Rats

Nephron ◽  
1996 ◽  
Vol 74 (4) ◽  
pp. 709-712 ◽  
Author(s):  
Tadasu Ikeda ◽  
Tazue Hoshino
Keyword(s):  
Protease Inhibitor ◽  
Urinary Albumin Excretion ◽  
Diabetic Rats ◽  
Urinary Albumin ◽  
Albumin Excretion ◽  
Streptozotocin Diabetic Rats

scholarly journals Aminoguanidine reduces regional albumin clearance but not urinary albumin excretion in streptozotocin-diabetic rats

Diabetologia ◽  
1994 ◽  
Vol 37 (1) ◽  
pp. 10-14 ◽  
Author(s):  
A. C. Nieuwenhuijzen Kruseman ◽  
H. A. J. Struijker Boudier ◽  
M. S. P. Huijberts ◽  
B. H. R. Wolffenbuttel ◽  
F. R. L. Crijns ◽  
...  
Keyword(s):  
Urinary Albumin Excretion ◽  
Diabetic Rats ◽  
Urinary Albumin ◽  
Albumin Excretion ◽  
Streptozotocin Diabetic Rats ◽  
Albumin Clearance

scholarly journals Aminoguanidine reduces regional albumin clearance but not urinary albumin excretion in streptozotocin-diabetic rats

Diabetologia ◽  
1994 ◽  
Vol 37 (1) ◽  
pp. 10-14 ◽  
Author(s):  
M. S. P. Huijberts ◽  
B. H. R. Wolffenbuttel ◽  
F. R. L. Crijns ◽  
A. C. Nieuwenhuijzen Kruseman ◽  
M. H. A. Bemelmans ◽  
...  
Keyword(s):  
Urinary Albumin Excretion ◽  
Diabetic Rats ◽  
Urinary Albumin ◽  
Albumin Excretion ◽  
Streptozotocin Diabetic Rats ◽  
Albumin Clearance

Effect of GH/IGF-I deficiency on long-term renal changes and urinary albumin excretion in diabetic dwarf rats

1997 ◽  
Vol 272 (5) ◽  
pp. E918-E924 ◽  
Author(s):  
H. Gronbaek ◽  
P. Volmers ◽  
S. F. Bjorn ◽  
R. Osterby ◽  
H. Orskov ◽  
...  
Keyword(s):  
Diabetic Kidney Disease ◽  
Urinary Albumin Excretion ◽  
Diabetic Rats ◽  
Urinary Albumin ◽  
Albumin Excretion ◽  
Igf I ◽  
Renal Changes ◽  
Rat Strain ◽  
Intact Rats

Growth hormone (GH) and insulin-like growth factor I (IGF-I) may play a role in early diabetic renal and glomerular growth and in the later development of experimental diabetic kidney disease. Rats from a genetic GH/IGF-I-deficient dwarf rat strain were made streptozotocin diabetic and were compared with nondiabetic dwarf rats. GH/IGF-I-intact rats with and without diabetes served as controls. After 6 mo of diabetes, kidney weight and total glomerular volume increased significantly in GH/IGF-I-intact diabetic rats compared with the nondiabetic GH/IGF-I-intact rats (P < 0.05), whereas the diabetic dwarf rats had insignificant changes compared with dwarf control rats. By the end of the study, urinary albumin excretion (UAE) increased from similar base levels of approximately 15-20 micrograms/24 h to 473 +/- 52 (SE) micrograms/24 h in GH/IGF-I-intact diabetic rats compared with 151 +/- 32 micrograms/24 h in diabetic dwarf rats (P < 0.01). In conclusion, isolated GH/IGF-I deficiency reduces the degree of renal and glomerular hypertrophy and the increase in UAE after 6 mo of experimental diabetes in GH/IGF-I-deficient rats.

scholarly journals Effect of Combination Therapy with a Calcium Channel Blocker and an Angiotensin-Converting Enzyme Inhibitor on Renal Hypertrophy and Urinary Albumin Excretion in Diabetic Rats

2003 ◽  
Vol 4 (3) ◽  
pp. 191-199 ◽  
Author(s):  
Birgitte Nielsen ◽  
Henning Grønbæk ◽  
Ruth Østerby ◽  
Allan Flyvbjerg
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Channel Blocker ◽  
Urinary Albumin Excretion ◽  
Placebo Treatment ◽  
Diabetic Rats ◽  
Urinary Albumin ◽  
Converting Enzyme ◽  
Albumin Excretion

The objective of this study was to compare the effect of an angiotensin-converting enzyme (ACE) inhibitor and a calcium channel blocker on the development of renal changes in diabetic rats. Diabetes was induced by an intravenous injection of streptozotocin in normotensive Wistar rats. Treatment was commenced immediately in 1 set of rats with 4 treatment arms: nitrendipine (250 mg/kg fodder), enalapril (35 mg/L drinking water), both treatments in combination, or placebo. Treatment was continued for 9 weeks. Another set of rats was left with untreated diabetes for 3 months followed by 7 weeks treatment as above. When starting treatment right after induction of diabetes, nitrendipine significantly reduced urinary albumin excretion (UAE) to the nondiabetic level (P< .05) without reducing blood pressure (BP), whereas enalapril failed to significantly reduce UAE despite a reduction in BP. Combining the two treatments showed no further reduction in UAE compared to monotherapy with nitrendipine, despite a lower BP. When leaving diabetic rats untreated for 3 months, only the coadministration of nitrendipine and enalapril showed a significant reduction in UAE compared to monotherapy and placebo treatment, but showed no significant effect on BP.

scholarly journals Octreotide administration in diabetic rats: Effects on renal hypertrophy and urinary albumin excretion

1992 ◽  
Vol 41 (4) ◽  
pp. 805-812 ◽  
Author(s):  
Allan Flyvbjerg ◽  
Sally M. Marshall ◽  
Jan Frystyk ◽  
Klavs W. Hansen ◽  
Alan G. Harris ◽  
...  
Keyword(s):  
Urinary Albumin Excretion ◽  
Diabetic Rats ◽  
Urinary Albumin ◽  
Renal Hypertrophy ◽  
Albumin Excretion

Effect of TNF-α inhibition on urinary albumin excretion in experimental diabetic rats

2007 ◽  
Vol 44 (4) ◽  
pp. 215-218 ◽  
Author(s):  
Yuji Moriwaki ◽  
Taku Inokuchi ◽  
Asako Yamamoto ◽  
Tsuneyoshi Ka ◽  
Zenta Tsutsumi ◽  
...  
Keyword(s):  
Urinary Albumin Excretion ◽  
Diabetic Rats ◽  
Urinary Albumin ◽  
Albumin Excretion ◽  
Tnf Α

scholarly journals Regulation of renal 12(S)-hydroxyeicosatetraenoic acid in diabetes by angiotensin AT1 and AT2 receptors

2008 ◽  
Vol 295 (5) ◽  
pp. R1473-R1478 ◽  
Author(s):  
Emaad M. Abdel-Rahman ◽  
Peter M. Abadir ◽  
Helmy M. Siragy
Keyword(s):  
Angiotensin Ii ◽  
Normal Control ◽  
Interstitial Fluid ◽  
Urinary Albumin Excretion ◽  
Diabetic Rats ◽  
Urinary Albumin ◽  
Receptor Blockade ◽  
Ang Ii ◽  
Hydroxyeicosatetraenoic Acid ◽  
Albumin Excretion

Diabetes is associated with increased production of 12(S)-hydroxyeicosatetraenoic acid [12(S)-HETE]. The mechanisms involved in this process remain unclear. We hypothesized that hyperglycemia and angiotensin II (ANG II) regulate renal 12(S)-HETE production via a balance between angiotensin AT1 and AT2 receptors activities. Using a microdialysis technique, renal interstitial fluid (RIF) levels of ANG II and 12(S)-HETE were monitored in normal control and streptozotocin-induced diabetic rats at baseline and then weekly thereafter for 12 wk. In a second group of normal and diabetic rats, 3 wk after development of diabetes, we monitored RIF 12(S)-HETE levels in response to acute AT1 receptor blockade with valsartan or AT2 receptor blockade with PD123319 individually or combined. Two weeks after induction of diabetes there was a 404% increase in ANG II ( P < 0.05), a 149% increase in 12S-HETE ( P < 0.05), and a 649% increase in urinary albumin excretion ( P < 0.05). These levels remained elevated throughout the study. PD123319 given alone had no effect on 12(S)-HETE. Valsartan decreased 12(S)-HETE by 61.6% ( P < 0.0001), a response that was abrogated when PD123319 was given with valsartan. These data demonstrate that hyperglycemia increases renal ANG II and 12(S)-HETE levels. The increase in 12(S)-HETE is mediated via AT1 receptor. The attenuation of the effects of AT1 receptor blockade by PD123319 suggests that AT2 receptor contributes to the downregulation of renal 12(S)-HETE production.

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