Epithelial Sodium Channel Inhibition by Amiloride on Blood Pressure and Cardiovascular Disease Risk in Young Prehypertensives. Issue 1 (31st October 2013)

• Record Type: Journal Article
• Authors: Bhagatwala, Jigar; Harris, Ryan A.; Parikh, Samip J.; Zhu, Haidong; Huang, Ying; Kotak, Ishita; Seigler, Nichole; Pierce, Gary L.; Egan, Brent M.; Dong, Yanbin
• Is Part Of: Journal of clinical hypertension. Volume 16:Issue 1(2014:Jan.)
• Page Start: 47
• Page End: 53
• Publication Date: 2013-10-31
• Subjects: Hypertension -- Periodicals; 616.132
• DOI: 10.1111/jch.12218
• Languages: English
• ISSNs: 1524-6175

Abstract

<abstract abstract-type="main" id="jch12218-abs-0001"> <title> <x xml:space="preserve">Abstract</x> </title> <p>Overactivity of the epithelial sodium channel (ENaC) is considered to be one mechanism underlying obesity‐related blood pressure (BP) elevation. In an open‐labeled, nonplacebo‐controlled clinical trial (Clinicaltrials.gov: NCT‐01308983), the authors aimed to comprehensively evaluate the effects of amiloride monotherapy, an ENaC 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/m². 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.</p> </abstract>