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

The present studies examine the consequences of the hemodynamic change s associated with approximate to 5/6 renal ablation in the spontaneous ly hypertensive rat (SHR), a strain that normally does not exhibit evi dence of vascular and/or glomerular injury until late in life despite significant hypertension. Control SHR with intact renal mass demonstra ted normal renal autoregulation and an absence of vascular or glomerul ar injury. Renal mass reduction resulted in an initial expected decrea se in renal blood flow to the remnant kidney at 5 days (2.8+/-0.3 mL/m in) compared with control SHR (8.1+/-0.7 mL/min) at a mean arterial pr essure of approximately 160 mm Hg (P<.01). By 10 to 14 days after rena l 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 arteriole s had also developed by 10 to 14 days after approximate to 5/6 renal a blation in a pattern similar to that observed in ''malignant'' hyperte nsion, despite systolic blood pressures that were not significantly di fferent from those in control SHR (168.2+/-6.4 versus 165.6+/-4.7 mm H g). An additional group of SHR that were made normotensive with a trip le-therapy antihypertensive regimen before and after approximate to 5/ 6 renal ablation also exhibited hemodynamic changes similar to those i n the untreated rats at 10 to 14 days but did not develop significant vascular or glomerular injury. These data suggest that the vasodilatio n and loss of protective autoregulation associated with 5/6 renal abla tion result in the acute transmission of preexistent hypertension to t he renal vasculature and the rapid development df severe vascular inju ry.