Abstract：
:The effect of captopril, an angiotensin-converting enzyme inhibitor, on the progression of chronic renal disease was studied in rats subjected to partial nephrectomy. Following ablation of approximately 70% of their renal mass, rats were divided into three treatment groups: group I received a placebo treatment; group II received daily po administrations of captopril; group III received captopril at the same dosage schedule as group II, but the drug was not given for 4 weeks in the middle of the treatment period. Measurements of renal function were performed at 4-week intervals, and light microscopic evaluation of the remnant kidneys was performed following 19 weeks of treatment. Deterioration of renal function, as measured by endogenous creatinine clearance, plasma creatinine, and plasma urea nitrogen, progressed more rapidly in group I than the other two groups. Twenty-four-hour urinary protein excretion was higher in group I than the others, except in group III following the 4-week period when captopril was not administered. Morphologic damage in the remnant kidney was significantly greater in group I than group II (p = 0.007). The renal lesions in the rats of group III were intermediate in severity. Histopathologic ranking of the remnant kidneys was correlated with antemortem laboratory parameters (r greater than or equal to 0.50; p less than 0.05). In a second experiment, similarly nephrectomized rats receiving po captopril daily had significantly longer survival, at 260 days, postnephrectomy than rats receiving a placebo (p = 0.0045). We conclude that captopril retards the progression of renal damage and increases survival time in this model of chronic renal disease. The mechanism may involve the alteration of potentially harmful intraglomerular hemodynamic changes which occur in the remnant kidney model.
journal_name
Toxicol Appl Pharmacoljournal_title
Toxicology and applied pharmacologyauthors
Hall RL,Wilke WL,Fettman MJdoi
10.1016/0041-008x(85)90397-7subject
Has Abstractpub_date
1985-09-30 00:00:00pages
517-26issue
3eissn
0041-008Xissn
1096-0333journal_volume
80pub_type
杂志文章abstract：:Thymic lymphoma/leukemia is the major cause of death in B6C3F1 mice chronically exposed to 1,3-butadiene (BD). Similar to radiation-induced murine thymic lymphoma, the bone marrow is also a major target organ. Because of the association of murine thymic lymphoma with endogenous type-C murine leukemia retroviruses (MuL...
journal_title：Toxicology and applied pharmacology
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journal_title：Toxicology and applied pharmacology
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journal_title：Toxicology and applied pharmacology
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journal_title：Toxicology and applied pharmacology
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journal_title：Toxicology and applied pharmacology
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更新日期：1987-02-01 00:00:00
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journal_title：Toxicology and applied pharmacology
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journal_title：Toxicology and applied pharmacology
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journal_title：Toxicology and applied pharmacology
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journal_title：Toxicology and applied pharmacology
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更新日期：2004-12-01 00:00:00
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journal_title：Toxicology and applied pharmacology
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更新日期：2014-10-15 00:00:00
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journal_title：Toxicology and applied pharmacology
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journal_title：Toxicology and applied pharmacology
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journal_title：Toxicology and applied pharmacology
pub_type： 杂志文章
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pub_type： 杂志文章
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journal_title：Toxicology and applied pharmacology
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更新日期：2000-09-15 00:00:00
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journal_title：Toxicology and applied pharmacology
pub_type： 杂志文章,评审
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更新日期：2013-04-15 00:00:00
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journal_title：Toxicology and applied pharmacology
pub_type： 杂志文章
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更新日期：1995-12-01 00:00:00
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journal_title：Toxicology and applied pharmacology
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journal_title：Toxicology and applied pharmacology
pub_type： 杂志文章
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journal_title：Toxicology and applied pharmacology
pub_type： 杂志文章,评审
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更新日期：2004-03-15 00:00:00
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journal_title：Toxicology and applied pharmacology
pub_type： 杂志文章
doi：10.1016/j.taap.2007.03.030
更新日期：2007-06-15 00:00:00
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journal_title：Toxicology and applied pharmacology
pub_type： 杂志文章
doi：10.1016/0041-008x(84)90115-7
更新日期：1984-03-15 00:00:00
