Cellular calcium in ischemic acute renal failure: Role of calcium entry blockers

Abstract

Some of the aspects of the cell biology of renal ischemia will be discussed, particularly as they relate to cellular calcium. Since the degree and duration of ischemic injury are major determinants of the cell's response, it is important to define precisely these factors in any discussion of renal cell injury. In the present editorial the degree and duration of renal ischemia to be discussed will be those that result in a reversible model of ischemic ARF. In the dog and rat this involves 45 to 50 minutes of total renal pedicle clamping; a shorter or less complete insult generally does not cause ARF and longer periods generally cause irreversible ARF. In our laboratory the intrarenal infusion of norepinephrine (NE) to cause total renal ischemia for 40 minutes has also been shown to produce a reversible ischemic model of ARF. Since studies of the pathogenesis of the injury incriminate a vascular component in the initiation phase and tubular obstruction in the maintenance phase of ischemic ARF, this editorial will address the potential role of calcium in both vascular and epithelial tissue. The potential interaction is shown between the vascular injury and the tubular injury of ischemic ARF, both of which will be discussed in detail.