Differential effects of renin–angiotensin–aldosterone system inhibition, sympathoinhibition and diuretic therapy on endothelial function and blood pressure in obesity-related hypertension: a double-blind, placebo-controlled cross-over trial
Abstract
OBJECTIVES: The objective of this study is to determine the effects of renin-angiotensin-aldosterone system inhibition, sympathoinhibition and diuretic therapy on endothelial function and blood pressure in obesity-related hypertension. METHODS: A randomized, four-way, double-blind, crossover study in 31 adults with previously untreated obesity-related hypertension, in which the effects of 8 weeks' inhibition of the renin-angiotensin-aldosterone system (using aliskiren 300 mg), sympathoinhibition (using moxonidine 0.4 mg), diuretic therapy (using hydrochlorothiazide 25 mg) or placebo on flow-mediated dilation and 24-h blood pressure were compared. RESULTS: The median flow-mediated dilation during placebo was 4.0% [interquartile range (IQR) 2.9-5.5%] and was increased by aliskiren [0.81%, 95% confidence interval (CI) 0.02-1.79], but not by moxonidine (0.20%, 95% CI -0.46 to 1.03) or hydrochlorothiazide (0.39%, 95%CI -0.31%-1.26%). Similarly, compared with placebo, mean 24-h blood pressure was most reduced by aliskiren (-9.8/-6.3 mmHg) and to a lesser degree by hydrochlorothiazide (-5.9/-2.6 mmHg). Moxonidine did not significantly affect blood pressure despite reduction of muscle sympathetic nerve activity. Insulin sensitivity deteriorated during hydrochlorothiazide treatment and was unaffected by aliskiren or moxonidine. Unlike aliskiren and moxonidine, hydrochlorothiazide reduced urinary 8-iso-prostaglandin F2α-VI, a marker of oxidative stress. Vascular stiffness, systemic inflammation, leptin, adiponectin and other oxidative stress markers (plasma malondialdehyde, myeloperoxidase activity and urinary 8-hydroxydeoxyguanosine) were unaffected by treatment. CONCLUSION: Renin inhibition, but not sympathoinhibition or diuretic therapy, improves endothelial function and results in larger reductions of 24-h, office, and central blood pressure in obesity-related hypertension. This adds weight to the hypothesis that inhibition of the renin-angiotensin-aldosterone system is an effective first step in the treatment of obesity-related hypertension.
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Blockade of the RAAS with angiotensin II receptor blockers, ACE inhibitors, or renin inhibitors reduces blood pressure in patients with obesity and hypertension.
“As mentioned above, blockade of the RAAS with AngII receptor blockers, angiotensin-converting enzyme (ACE) inhibitors or renin inhibitors reduces BP in patients with obesity and hypertension64–66.”
From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [64]
Smaller clinical trials have clearly shown that angiotensin receptor blockers (ARBs), renin inhibitors, or angiotensin converting enzyme (ACE) inhibitors are effective in lowering BP in obese hypertensive patients.
“Although smaller clinical trials have clearly shown that angiotensin receptor blockers (ARBs), renin inhibitors, or angiotensin converting enzyme (ACE) inhibitors are effective in lowering BP in obese hypertensive patients46–48, there have been no large-scale clinical studies comparing the effectiveness of RAAS blockers in obese and lean hypertensive patients.”
From Obesity-Induced Hypertension: Interaction of Neurohumoral and Renal Mechanisms (2015) · cites this paper as [48]
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- Authors
- Dorresteijn, J. A. N., Schrover, I. M., Visseren, F. L. J., Scheffer, P. G., Oey, P. L., Danser, A. H. (., & Spiering, W.
- Affiliations
- University Medical Center Utrecht (NL)
- Amsterdam UMC Location Vrije Universiteit Amsterdam (NL)
- Erasmus MC (NL)
- Corresponding author
- Spiering, Wilko
- Venue
- Journal of Hypertension
- Published
- 2013-02
- Volume
- 31
- Issue
- 2
- Pages
- 393-403
- ISSN
- 0263-6352 (ISSN-L)
- OpenAlex
- W2088257585
- Cited by
- 50
- References
- 32
- Citations by year
- 2025: 3 · 2024: 4 · 2023: 1 · 2022: 4 · 2021: 2 · 2020: 3 · 2019: 5 · 2018: 2 · 2017: 5 · 2016: 6 · 2015: 4 · 2014: 8 · 2013: 3
- FWCI
- 3.09
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Hypertension (publishedVersion)
- PubMed (publishedVersion)
- Pure Amsterdam UMC (publishedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (submittedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Funders
- Julius Clinical
- Novartis Pharma
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Health and Disease Prevention
- Keywords
- obesity-related hypertension, renin-angiotensin-aldosterone system inhibition, aliskiren, sympathoinhibition, moxonidine, hydrochlorothiazide, diuretics, endothelial function, flow-mediated dilation, blood pressure, insulin sensitivity, oxidative stress, 8-isoprostane, vascular stiffness, systemic inflammation, leptin, adiponectin
- MeSH terms
- Diuretics, Double-Blind Method, Endothelium, Vascular, Female, Humans, Hydrochlorothiazide, Hypertension, Male, Middle Aged, Obesity, Placebos, Renin-Angiotensin System, Cross-Over Studies
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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