Lovastatin has Direct Renal Hemodynamic Effects in a Rodent Model

Abstract

Purpose Lovastatin, an HMG-CoA reductase inhibitor, has been shown to preserve renal function in models of chronic renal failure. We determined the effect of lovastatin on renal function and hemodynamics in normal nonpathologic kidneys in a rodent model. Materials and Methods Renal function was measured in anesthetized (Inactin) control rats (n = 13) and lovastatin-treated rats (15 mg./kg./day, 3 weeks, orally, n = 17). Renal blood flow was measured with an ultrasonic flowprobe, and glomerular filtration rate was measured by inulin clearance. The effect of lovastatin on pre- and postglomerular vessel diameters was also observed in a hydronephrotic kidney preparation by videomicroscopy. Results Lovastatin significantly increased (p less than 0.05) renal blood flow and glomerular filtration rate by 17 percent (3.4 plus/minus 0.2 ml./min./gram kidney weight (gKW) versus 2.9 plus/minus 0.2 ml./min./gKW) and 49 percent (0.67 plus/minus 0.04 ml./min./gKW versus 0.45 plus/minus 0.06 ml./min./gKW). The increase in renal blood flow was mediated by preglomerular vasolidation (expressed as percent increase from baseline diameter, n = 20), 25 percent in the interlobular artery and 20 percent in the afferent arteriole (p less than 0.05). Conclusions In addition to its known lipid-lowering properties, lovastatin has a direct renal hemodynamic effect, increasing renal blood flow and glomerular filtration rate in normal nonpathologic kidneys. Lovastatin's selective preglomerular vasodilation may account for the observed increase in renal blood flow and glomerular filtration rate. Accordingly, this additional hemodynamic effect may be useful in preserving renal function in models of chronic renal failure.