Key result
Furosemide treatment increased central blood pressure and water and sodium absorption via AQP2 and ENaC, likely as compensatory phenomena to antagonize water and sodium depletion.
Why the study?
Does amiloride or spironolactone reduce ambulatory and central blood pressure and alter tubular transport in healthy participants?
RCT
Double-blind
Crossover
Does amiloride or spironolactone reduce ambulatory and central blood pressure and alter tubular transport in healthy participants?
Furosemide treatment induces compensatory increases in water and sodium absorption via AQP2 and ENaC to antagonize depletion.
Furosemide may raise central BP in healthy adults; extends evidence for compensatory AQP2/ENaC activation.
We wanted to test the hypothesis that treatment with amiloride or spironolactone reduced ambulatory (ABP) and central blood pressure (CBP) and that tubular transport via ENaCγ and AQP2 was increased after furosemide treatment. During baseline conditions, there were no differences in ABP, CBP, renal tubular function, or plasma concentrations of vasoactive hormones. After furosemide treatment, an increase in CBP, CH(2)o, FE(Na), FE(K), u-AQP2/min, u-ENaCγ/min, PRC, p-Ang II, and p-Aldo was observed. The increases in water and sodium absorption via AQP2 and ENaC after furosemide treatment most likely are compensatory phenomena to antagonize water and sodium depletion.
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Matthesen et al. (2012) conducted an RCT in Healthy Participants. Amiloride or spironolactone, and furosemide vs. Placebo was evaluated on Ambulatory and central blood pressure, and tubular transport via ENaCγ and AQP2. Furosemide treatment increased central blood pressure and water and sodium absorption via AQP2 and ENaC, likely as compensatory phenomena to antagonize water and sodium depletion.
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