LOVASTATIN HAS DIRECT RENAL HEMODYNAMIC-EFFECTS IN A RODENT MODEL

Purpose: Lovastatin, an HMG-CoA reductase inhibitor, has been shown to preserve renal function in models of chronic renal failure. We determ ined the effect of lovastatin on renal function and hemodynamics in no rmal nonpathologic kidneys in a rodent model. Materials and Methods: R enal function was measured in anesthetized (Inactin) control rats (n=1 3) and lovastatin-treated rats (15 mg./kg./day, 3 weeks, orally, n=17) . Renal blood flow was measured with an ultrasonic flowprobe, and glom erular filtration rate was measured by inulin clearance. The effect of lovastatin on pre- and postglomerular vessel diameters was also obser ved in a hydronephrotic kidney preparation by videomicroscopy. Results : Lovastatin significantly increased (p<0.05) renal blood flow and glo merular filtration rate by 17% (3.4+/-0.2 ml./min./gram kidney weight (gKW) versus 2.9+/-0.2 ml./min./gKW) and 49% (0.67+/-0.04 ml./min./gKW versus 0.45+/-0.06 ml./min./gKW). The increase in renal blood flow wa s mediated by preglomerular vasodilation (expressed as percent increas e from baseline diameter, n=20), 25% in the interlobular artery and 20 % in the afferent arteriole (p<0.05). Conclusions: In addition to its known lipid-lowering properties, lovastatin has a direct renal hemodyn amic effect, increasing renal blood flow and glomerular filtration rat e in normal nonpathologic kidneys. Lovastatin's selective preglomerula r vasodilation may account for the observed increase in renal blood fl ow and glomerular filtration rate. Accordingly, this additional hemody namic effect may be useful in preserving renal function in models of c hronic renal failure.