Increase in collateral arterial endothelial cell proliferation induced by captopril after renal artery stenosis in the rat.

Studies to assess the role of blood pressure rise in the growth of the collateral arterial supply following renal artery stenosis were performed in 70 rats. Assessment of the proliferative response was made by coded reading of endothelial cell turnover following tritiated thymidine administration, 5 days after renal artery stenosis. Stenosis induced the anticipated brisk increase in endothelial cell turnover in arterial collaterals and in the ipsilateral renal vein, and ureteric epithelium. Blood pressure elevation did not appear to play the dominant role, as the proliferative response did not parallel blood pressure changes; moreover, neither bilateral renal artery stenosis, designed to enhance the hypertension, nor hydralazine administration, to reduce the blood pressure, influenced endothelial cell turnover. A contribution of elevated blood pressure to the vasoproliferative response, however, was not ruled out definitively in this study. Captopril, also administered to assess the same question, resulted in an enhanced endothelial cell proliferative response, both in frequency and in degree, an observation that became the central thrust of our study. The mechanism by which converting enzyme inhibitor modified endothelial cell turnover is not clear, but may well provide insight into the responsible factors.