Key result
In spontaneously hypertensive rats, inhibiting aminopeptidase N with PC-18 restored defective angiotensin II type 2-mediated natriuresis (urine sodium excretion increased from 0.05 to 0.11 µmol/min; P<0.05).
Why the study?
Does aminopeptidase N inhibition restore AT2R-mediated natriuresis in spontaneously hypertensive rats?
Population
Prehypertensive and hypertensive spontaneously hypertensive rats and age-matched Wistar-Kyoto rats
Comparison
Renal interstitial infusion of aminopeptidase N… vs Baseline measurements and age-matched…
Design
Preclinical
Authors
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Hypothesis-generating for aminopeptidase N inhibition in hypertension; prospective human trials needed before any clinical consideration.
Does aminopeptidase N inhibition restore AT2R-mediated natriuresis in spontaneously hypertensive rats?
p-value: p=<0.05
Inhibition of aminopeptidase N restores defective AT2R-mediated natriuresis in spontaneously hypertensive rats, highlighting a potential mechanism to address sodium retention in hypertension.
Padia et al. (2009) studied Hypertension. PC-18 (aminopeptidase N inhibitor) vs. Baseline / Wistar-Kyoto rats was evaluated on Urine sodium excretion rates (UNaV) (p=<0.05). In spontaneously hypertensive rats, inhibiting aminopeptidase N with PC-18 restored defective angiotensin II type 2-mediated natriuresis (urine sodium excretion increased from 0.05 to 0.11 µmol/min; P<0.05).
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