Effects of captopril on urinary excretion of albumin and prostaglandins in patients with diabetic nephropathy.

Y. Tajiri, F. Umeda, Toyoshi Inoguchi, M. Kunisaki, H. Nawata, H. Ninomiya, T. Asano

    Research output: Contribution to journalArticle

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    Abstract

    Recently the beneficial effects of captopril (angiotensin-converting-enzyme inhibitor) on diabetic nephropathy, especially proteinuria, have been reported by some investigators. The mechanism whereby proteinuria is reduced, however, have not been clarified yet. The present study was undertaken to evaluate the effects of captopril on urinary albumin excretion in relation to urinary prostaglandins (PGs) excretion in patients with non-insulin-dependent diabetes mellitus (NIDDM). Captopril (37.5 mg/day) was orally administered to 13 diabetic patients for an eight-week period. A single administration of captopril (12.5 mg) was performed in the same patients. The spot urine samples were collected in the early morning and 2 hr after the single administration of captopril. The albumin index (mg/gram-creatinine) was markedly decreased in eight patients (Group A) within four weeks, but no decrease was found in five patients (Group B). Furthermore, in Group A, by the single administration of captopril urinary excretions of 6-keto-PCF1 alpha (a stable metabolite of PGI2) and PGE2 were significantly (p less than 0.05) increased while urinary TXB2 (a stable metabolite of TXA2) excretion did not change significantly. The urinary 6-keto-PGF1 alpha/TXB2 ratio, which is significantly (p less than 0.05) low in diabetic patients was significantly (p less than 0.01) increased up to the normal value in Group A. In Group B, however, there were no significant changes in urinary PGs excretion. These results suggest that captopril enhances the production of intrarenal vasodilatory PGs such as PGI2 and PGE2, which may be deeply involved in the reduction of intraglomerular capillary pressure and urinary protein excretion in diabetic patients.

    Original languageEnglish
    Pages (from-to)145-150
    Number of pages6
    JournalDiabetes research (Edinburgh, Lothian)
    Volume13
    Issue number3
    Publication statusPublished - Jan 1 1990

    Fingerprint

    Captopril
    Diabetic Nephropathies
    Prostaglandins
    Albumins
    Epoprostenol
    Proteinuria
    Dinoprostone
    6-Ketoprostaglandin F1 alpha
    Angiotensin-Converting Enzyme Inhibitors
    Type 2 Diabetes Mellitus
    Creatinine
    Reference Values
    Research Personnel
    Urine
    Pressure
    Proteins

    All Science Journal Classification (ASJC) codes

    • Endocrinology
    • Internal Medicine
    • Endocrinology, Diabetes and Metabolism

    Cite this

    Tajiri, Y., Umeda, F., Inoguchi, T., Kunisaki, M., Nawata, H., Ninomiya, H., & Asano, T. (1990). Effects of captopril on urinary excretion of albumin and prostaglandins in patients with diabetic nephropathy. Diabetes research (Edinburgh, Lothian), 13(3), 145-150.

    Effects of captopril on urinary excretion of albumin and prostaglandins in patients with diabetic nephropathy. / Tajiri, Y.; Umeda, F.; Inoguchi, Toyoshi; Kunisaki, M.; Nawata, H.; Ninomiya, H.; Asano, T.

    In: Diabetes research (Edinburgh, Lothian), Vol. 13, No. 3, 01.01.1990, p. 145-150.

    Research output: Contribution to journalArticle

    Tajiri, Y, Umeda, F, Inoguchi, T, Kunisaki, M, Nawata, H, Ninomiya, H & Asano, T 1990, 'Effects of captopril on urinary excretion of albumin and prostaglandins in patients with diabetic nephropathy.', Diabetes research (Edinburgh, Lothian), vol. 13, no. 3, pp. 145-150.
    Tajiri Y, Umeda F, Inoguchi T, Kunisaki M, Nawata H, Ninomiya H et al. Effects of captopril on urinary excretion of albumin and prostaglandins in patients with diabetic nephropathy. Diabetes research (Edinburgh, Lothian). 1990 Jan 1;13(3):145-150.
    Tajiri, Y. ; Umeda, F. ; Inoguchi, Toyoshi ; Kunisaki, M. ; Nawata, H. ; Ninomiya, H. ; Asano, T. / Effects of captopril on urinary excretion of albumin and prostaglandins in patients with diabetic nephropathy. In: Diabetes research (Edinburgh, Lothian). 1990 ; Vol. 13, No. 3. pp. 145-150.
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    AU - Ninomiya, H.

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    N2 - Recently the beneficial effects of captopril (angiotensin-converting-enzyme inhibitor) on diabetic nephropathy, especially proteinuria, have been reported by some investigators. The mechanism whereby proteinuria is reduced, however, have not been clarified yet. The present study was undertaken to evaluate the effects of captopril on urinary albumin excretion in relation to urinary prostaglandins (PGs) excretion in patients with non-insulin-dependent diabetes mellitus (NIDDM). Captopril (37.5 mg/day) was orally administered to 13 diabetic patients for an eight-week period. A single administration of captopril (12.5 mg) was performed in the same patients. The spot urine samples were collected in the early morning and 2 hr after the single administration of captopril. The albumin index (mg/gram-creatinine) was markedly decreased in eight patients (Group A) within four weeks, but no decrease was found in five patients (Group B). Furthermore, in Group A, by the single administration of captopril urinary excretions of 6-keto-PCF1 alpha (a stable metabolite of PGI2) and PGE2 were significantly (p less than 0.05) increased while urinary TXB2 (a stable metabolite of TXA2) excretion did not change significantly. The urinary 6-keto-PGF1 alpha/TXB2 ratio, which is significantly (p less than 0.05) low in diabetic patients was significantly (p less than 0.01) increased up to the normal value in Group A. In Group B, however, there were no significant changes in urinary PGs excretion. These results suggest that captopril enhances the production of intrarenal vasodilatory PGs such as PGI2 and PGE2, which may be deeply involved in the reduction of intraglomerular capillary pressure and urinary protein excretion in diabetic patients.

    AB - Recently the beneficial effects of captopril (angiotensin-converting-enzyme inhibitor) on diabetic nephropathy, especially proteinuria, have been reported by some investigators. The mechanism whereby proteinuria is reduced, however, have not been clarified yet. The present study was undertaken to evaluate the effects of captopril on urinary albumin excretion in relation to urinary prostaglandins (PGs) excretion in patients with non-insulin-dependent diabetes mellitus (NIDDM). Captopril (37.5 mg/day) was orally administered to 13 diabetic patients for an eight-week period. A single administration of captopril (12.5 mg) was performed in the same patients. The spot urine samples were collected in the early morning and 2 hr after the single administration of captopril. The albumin index (mg/gram-creatinine) was markedly decreased in eight patients (Group A) within four weeks, but no decrease was found in five patients (Group B). Furthermore, in Group A, by the single administration of captopril urinary excretions of 6-keto-PCF1 alpha (a stable metabolite of PGI2) and PGE2 were significantly (p less than 0.05) increased while urinary TXB2 (a stable metabolite of TXA2) excretion did not change significantly. The urinary 6-keto-PGF1 alpha/TXB2 ratio, which is significantly (p less than 0.05) low in diabetic patients was significantly (p less than 0.01) increased up to the normal value in Group A. In Group B, however, there were no significant changes in urinary PGs excretion. These results suggest that captopril enhances the production of intrarenal vasodilatory PGs such as PGI2 and PGE2, which may be deeply involved in the reduction of intraglomerular capillary pressure and urinary protein excretion in diabetic patients.

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