Hypertension, Vol 24, 309-316, Copyright © 1994 by American Heart Association
AK Bidani, KA Griffin, W Plott and MM Schwartz
The present studies examine the consequences of the hemodynamic changes
associated with approximately 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 approximately 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 approximately 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 approximately 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.(ABSTRACT TRUNCATED AT 250 WORDS)
ARTICLES
Renal ablation acutely transforms 'benign' hypertension to 'malignant' nephrosclerosis in hypertensive rats
Department of Medicine, Loyola University, Maywood, Ill.
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