Objective: Using a rat in vivo hydronephrotic model we studied the acute and chronic effects of the short-acting calcium channel blocker nifedipine on renal microcirculation. Background: Antihypertensive drugs such as angiotensin-converting enzyme (ACE) inhibitors that dilate both preglomerular afferent and postglomerular efferent arterioles are thought to have a renal protective effect; calcium channel blockers, in contrast, are thought to elevate glomerular pressure and aggravate glomerular damage. Because slow- release nifedipine has been shown to have beneficial effects on the course of glomerular disease, we hypothesized that nifedipine has differential effects on renal microcirculation, depending on its mode of action. Methods: Hydronephrosis was induced by permanent ligation of the left ureter in spontaneously hypertensive rats. Under a light microscope, renal microcirculation was observed directly by spreading out the hydronephrotic kidney as a thin sheet. The effects of nifedipine or imidapril on renal microcirculation were analyzed by importing the microscopic images into a computer. Results: Intravenous injection of nifedipine 10 μg/kg transiently decreased blood pressure and dilated afferent arterioles (from 14% to 19% in diameter at 10 minutes after injection). In contrast, nifedipine did not affect efferent arteriolar diameter. The ACE inhibitor imidapril 50 μg/kg was administered in the same manner for reference; it dilated both afferent and efferent arterioles in this experimental model (17% increase at 20 minutes and 12% at 10 minutes, respectively). When administered into an organ bath, nifedipine dilated both afferent (from 15% to 20% at both 10-8M and 10-6M) and efferent arterioles (15% at 10-10M and 20% at 10-6M). Conclusions: These results show that when nifedipine is administered to the renal microvasculature in a stable manner, it acts on the renal microcirculation in the same fashion as do ACE inhibitors.
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