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1 Department of Pediatric Surgery, Erasmus University Medical School, 3000 DR Rotterdam, The Netherlands; and 2 Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226
The
responses to changes in renal perfusion pressure (RPP) were compared in
12-wk-old fawn-hooded hypertensive (FHH), fawn-hooded low blood
pressure (FHL), and August Copenhagen Irish (ACI) rats to determine
whether autoregulation of renal blood flow (RBF) is altered in the FHH
rat. Mean arterial pressure was significantly higher in conscious,
chronically instrumented FHH rats than in FHL rats (121 ± 4 vs. 109 ± 6 mmHg). Baseline arterial pressures measured in
ketamine-Inactin-anesthetized rats averaged 147 ± 2 mmHg
(n = 9) in FHH, 132 ± 2 mmHg
(n = 10) in FHL, and 123 ± 4 mmHg
(n = 9) in ACI rats. Baseline RBF was
significantly higher in FHH than in FHL and ACI rats and averaged
9.6 ± 0.7, 7.4 ± 0.5, and 7.8 ± 0.9 ml · min
1 · g
kidney wt
1, respectively.
RBF was autoregulated in ACI and FHL but not in FHH rats.
Autoregulatory indexes in the range of RPPs from 100 to 150 mmHg
averaged 0.96 ± 0.12 in FHH vs. 0.42 ± 0.04 in FHL and
0.30 ± 0.02 in ACI rats. Glomerular filtration rate was 20-30% higher in FHH than in FHL and ACI rats. Elevations in RPP from 100 to
150 mmHg increased urinary protein excretion in FHH rats from 27 ± 2 to 87 ± 3 µg/min, whereas it was not significantly altered in FHL or ACI rats. The percentage of glomeruli exhibiting histological evidence of injury was not significantly different in the
three strains of rats. These results indicate that autoregulation of
RBF is impaired in FHH rats before the development of
glomerulosclerosis and suggest that an abnormality in the control of
renal vascular resistance may contribute to the development of
proteinuria and renal failure in this strain of rats.
renal hemodynamics; renal vasculature; pressure proteinuria; glomerulus; kidney disease
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