RENAL ABLATION ACUTELY TRANSFORMS BENIGN HYPERTENSION TO MALIGNANT NEPHROSCLEROSIS IN HYPERTENSIVE RATS

The present studies examine the consequences of the hemodynamic changes associated with approximate to 5/6 renal ablation in the spontaneously hypertensive rat (SHR), a strain that normally does not exhibit evidence of vascular and/or glomerular injury until late in life despite significant hypertension. Control SHR with intact renal mass demonstrated normal renal autoregulation and an absence of vascular or glomerular injury. Renal mass reduction resulted in an initial expected decrease in renal blood flow to the remnant kidney at 5 days (2.8+/-0.3 mL/min) compared with control SHR (8.1+/-0.7 mL/min) at a mean arterial pressure of approximately 160 mm Hg (P<.01). By 10 to 14 days after renal ablation, marked renal vasodilation was observed (renal blood flow 8.3+/-0.8 mL/min at mean arterial pressure of approximate to 160 mm Hg) along with severe impairment of autoregulatory ability. Striking and florid vascular injury to interlobular arteries and afferent arterioles had also developed by 10 to 14 days after approximate to 5/6 renal ablation in a pattern similar to that observed in ''malignant'' hypertension, despite systolic blood pressures that were not significantly different from those in control SHR (168.2+/-6.4 versus 165.6+/-4.7 mm Hg). An additional group of SHR that were made normotensive with a triple-therapy antihypertensive regimen before and after approximate to 5/6 renal ablation also exhibited hemodynamic changes similar to those in the untreated rats at 10 to 14 days but did not develop significant vascular or glomerular injury. These data suggest that the vasodilation and loss of protective autoregulation associated with 5/6 renal ablation result in the acute transmission of preexistent hypertension to the renal vasculature and the rapid development df severe vascular injury.