Increased collateral arterial and venous endothelial cell turnover after renal artery stenosis in the dog.

Renal artery stenosis was induced in dogs and collateral arterial formation assessed by serial angiography and histology. Endothelial cell turnover was estimated by radioautography in five normal and five collateral-forming kidneys 18-39 days following stenosis with tritiated thymidine. Normal arterial endothelial labeling was 0.1% with a highly significant (p less than 0.0005), 55-fold increase in endothelial labeling in arterial collateral vessels. A smaller but statistically significant increase in the labeling index was also found in endothelial cells of the renal vein, from a normal of 0.065% to 0.4% (p less than 0.005). An excellent correlation was found between endothelial cell labeling in small arteries and the renal veins (r = 0.97; p less than 0.01). A marked increase in epithelial cell labeling of the ureters draining the stenotic kidneys was also evident (p less than 0.005). Thus, collateral vessel development is characterized by active DNA synthesis in cellular elements, and a humoral factor is implicated in the vascular response.