Effects of benidipine, a calcium antagonist, on urinary kallikrein excretion and renal impairment in experimental diabetes

Kazunori Yoshida, Masahiro Kohzuki, Minoru Yasujima, Masayuki Kanazawa, Keishi Abe

研究成果: Article査読

22 被引用数 (Scopus)

抄録

Objective To assess the long-term effects of different antihypertensive agents on urinary protein excretion and kallikrein excretion in diabetic rats with renal impairment Methods Uninephrectomized streptozotocin diabetic Wistar-Kyoto rats were randomly assigned to receive vehicle, a calcium antagonist (benidipine) or an angiotensin converting enzyme inhibitor (captopril) for up to 12 weeks. Active kallikrein was determined by its kininogenase activity, and generated kinins were measured by radioimmunoassay. Total kallikrein was also determined by measuring kininogenase activity after inactive kallikrein had been activated with trypsin. Results Urinary protein excretion increased significantly in diabetic rats compared with non-diabetic rats. Urinary active kallikrein excretion was significantly reduced in diabetic rats, whereas urinary total kallikrein excretion was unchanged, resulting in a reduced percentage of active to total kallikrein compared with that in non-diabetic rats. Benidipine and captopril reduced blood pressure and attenuated the development of diabetic renal impairment in a similar manner. However, only benidipine attenuated the decreases in urinary active kallikrein excretion and the ratio of active to total kallikrein in diabetic rats. Conclusions Although pathophysiological relevance of impaired urinary kallikrein activation to the development of diabetic renal impairment remains to be determined, our result might suggest a new mechanism by which calcium antagonists protect the kidney from diabetic renal impairment.

本文言語English
ページ(範囲)215-222
ページ数8
ジャーナルJournal of hypertension
14
2
DOI
出版ステータスPublished - 1996

ASJC Scopus subject areas

  • 内科学
  • 生理学
  • 循環器および心血管医学

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