Open AccessEpithelial Sodium Channel Inhibition by Amiloride on Blood Pressure and Cardiovascular Disease Risk in Young Prehypertensives
Author(s) -
Bhagatwala Jigar,
Harris Ryan A.,
Parikh Samip J.,
Zhu Haidong,
Huang Ying,
Kotak Ishita,
Seigler Nichole,
Pierce Gary L.,
Egan Brent M.,
Dong Yanbin
Publication year - 2014
Publication title -
the journal of clinical hypertension
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 67
eISSN - 1751-7176
pISSN - 1524-6175
DOI - 10.1111/jch.12218
Subject(s) - medicine , amiloride , blood pressure , epithelial sodium channel , prehypertension , pulse wave velocity , endocrinology , body mass index , cardiology , aldosterone , sodium , chemistry , organic chemistry
Overactivity of the epithelial sodium channel ( EN a C ) is considered to be one mechanism underlying obesity‐related blood pressure ( BP ) elevation. In an open‐labeled, nonplacebo‐controlled clinical trial ( C linicaltrials.gov: NCT ‐01308983), the authors aimed to comprehensively evaluate the effects of amiloride monotherapy, an EN a C blocker, on BP and cardiovascular risk in young adults with prehypertension (n=17). The mean body mass index of participants was 28.45±1.30 kg/m 2 . Following 10 mg daily amiloride for 4 weeks, peripheral systolic BP ( SBP ), central SBP , and carotid‐radial pulse wave velocity were significantly reduced by −7.06±2.25 mm Hg, −7.68±2.56 mm Hg, and −0.72±0.33 m/s, respectively, whereas flow‐mediated dilation was significantly increased by 2.2±0.9%. Following amiloride monotherapy for 4 weeks, a significant increase in serum aldosterone was observed (5.85±2.45 ng/dL). ENaC inhibition by amiloride may be used as an early intervention to halt the progression to full hypertension and cardiovascular disease in young adults with prehypertension.