The role of the calcium-dependent enzymes nitric oxide synthase and calpain in hypoxia-induced proximal tubule injury

被引：17

作者：

Edelstein, CL ^{[1
]}

Yaqoob, MM ^{[1
]}

Schrier, RW ^{[1
]}

机构：

[1] UNIV COLORADO,SCH MED,DEPT MED,DENVER,CO 80262

来源：

RENAL FAILURE | 1996年 / 18卷 / 03期

关键词：

D O I：

10.3109/08860229609052821

中图分类号：

R5 [内科学]; R69 [泌尿科学（泌尿生殖系疾病）];

学科分类号：

1002 ; 100201 ;

摘要：

A role of cytoplasmic free calcium [Ca2+](i) in hypoxia-induced proximal tubule damage has been proposed. To further investigate the role of [Ca2+](i) in mediating hypoxic proximal tubular injury, a video imaging technique has been developed in which [Ca2+](i) can be measured simultaneously, with propidium iodide (PI) staining of nuclei as an index of hypoxia-induced membrane damage. Hypoxia in rat proximal tubules is associated with a significant rise in [Ca2+](i) which precedes evidence of membrane damage as assessed by PI staining. This rise in [Ca2+](i) activates calpain, a Ca2+-dependent cysteine protease, and constitutive nitric oxide synthase (NOS), the Ca2+-dependent form of NOS. Inhibition of either calpain or nitric oxide synthase provides marked cytoprotection against hypoxic proximal tubular injury. These observations are consistent with the early rise in [Ca2+](i) initiating hypoxic injury by activating NOS and calpain.

引用

页码：501 / 511

页数：11

共 69 条

[11] NITRIC-OXIDE STIMULATES THE ADP-RIBOSYLATION OF ACTIN IN HUMAN NEUTROPHILS [J].