Key result
Proximal tubule fluid reabsorption was significantly lower in spontaneously hypertensive rats compared to Wistar-Kyoto rats (1.1 vs 2.3 nL/min per mm; P<0.001) and was normalized by NADPH oxidase inhibition.
Why the study?
Does NADPH oxidase inhibition improve proximal tubule fluid reabsorption in spontaneously hypertensive rats?
Population
Adult spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats (n=9 to 11 per group)
Comparison
NADPH oxidase inhibitor apocynin, small… vs Untreated SHR and WKY rats
Design
Preclinical
Authors
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Does not support clinical translation; leaves open NADPH oxidase inhibition as a hypertension target in humans.
Does NADPH oxidase inhibition improve proximal tubule fluid reabsorption in spontaneously hypertensive rats?
Absolute Event Rate: 1.1% vs 2.3%
p-value: p=<0.001
Superoxide generated by NADPH oxidase inhibits proximal tubule fluid reabsorption in spontaneously hypertensive rats, suggesting that redox balance regulates fluid homeostasis in the hypertensive kidney.
Panico et al. (2009) studied Hypertension (animal model). NADPH oxidase inhibition (Apocynin or siRNA for p22phox) vs. Untreated or WKY rats was evaluated on Proximal tubule fluid reabsorption (Jv) (p=<0.001). Proximal tubule fluid reabsorption was significantly lower in spontaneously hypertensive rats compared to Wistar-Kyoto rats (1.1 vs 2.3 nL/min per mm; P<0.001) and was normalized by NADPH oxidase inhibition.
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