Liraglutide Promotes Natriuresis but Does Not Increase Circulating Levels of Atrial Natriuretic Peptide in Hypertensive Subjects With Type 2 Diabetes
Abstract
OBJECTIVE: GLP-1 receptor (GLP-1R) agonists induce natriuresis and reduce blood pressure (BP) through incompletely understood mechanisms. We examined the effects of acute and 21-day administration of liraglutide on plasma atrial natriuretic peptide (ANP), urinary sodium excretion, office and 24-h BP, and heart rate (HR). RESEARCH DESIGN AND METHODS: Liraglutide or placebo was administered for 3 weeks to hypertensive subjects with type 2 diabetes in a double-blinded, randomized, placebo-controlled crossover clinical trial in the ambulatory setting. End points included within-subject change from baseline in plasma ANP, Nt-proBNP, office BP, and HR at baseline and over 4 h following a single dose of liraglutide (0.6 mg) and after 21 days of liraglutide (titrated to 1.8 mg) versus placebo administration. Simultaneous 24-h ambulatory BP and HR monitoring and 24-h urine collections were measured at baseline and following 21 days of treatment. RESULTS: Plasma ANP levels did not change significantly after acute (+16.72 pg/mL, P = 0.24, 95% CI [-12.1, +45.5] at 2 h) or chronic (-17.42 pg/mL, 95% CI [-36.0, +1.21] at 2 h) liraglutide administration. Liraglutide significantly increased 24-h and nighttime urinary sodium excretion; however, 24-h systolic BP was not significantly different. Small but significant increases in 24-h and nighttime diastolic BP and HR were observed with liraglutide. Body weight, HbA1c, and cholesterol were lower, and office-measured HR was transiently increased (for up to 4 h) with liraglutide administration. CONCLUSIONS: Sustained liraglutide administration for 3 weeks increases urinary sodium excretion independent of changes in ANP or BP in overweight and obese hypertensive patients with type 2 diabetes.
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GLP-1RA potentially further compromise fluid homeostasis by increasing renal sodium excretion.
“GLP-1RA potentially further compromise fluid homeostasis by increasing renal sodium excretion”
From Safety of Semaglutide (2021) · cites this paper as [116]
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- Authors
- Lovshin, J. A., Barnie, A., DeAlmeida, A., Logan, A., Zinman, B., & Drucker, D. J.
- Affiliations
- Mount Sinai Hospital (CA)
- Corresponding author
- Drucker, Daniel J.
- Venue
- Diabetes Care
- Publisher
- American Diabetes Association
- Published
- 2014-11-20
- Volume
- 38
- Issue
- 1
- Pages
- 132-139
- ISSN
- 0149-5992 (ISSN-L)
- 1935-5548
- OpenAlex
- W2158742250
- Cited by
- 168
- References
- 25
- Citations by year
- 2026: 2 · 2025: 11 · 2024: 16 · 2023: 12 · 2022: 12 · 2021: 18 · 2020: 15 · 2019: 16 · 2018: 14 · 2017: 19 · 2016: 23 · 2015: 9
- FWCI
- 13.60
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Diabetes Care (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Heart Failure Treatment and Management
- Keywords
- liraglutide, GLP-1 receptor agonists, sodium excretion, atrial natriuretic peptide, hypertension, type 2 diabetes, blood pressure, heart rate, NT-proBNP, ambulatory blood pressure monitoring
- MeSH terms
- Glucagon-Like Peptide-1 Receptor, Liraglutide, Adult, Aged, Blood Pressure, Body Weight, Diabetes Mellitus, Type 2, Double-Blind Method, Female, Heart Rate, Humans, Hypertension, Male, Middle Aged, Natriuresis, Atrial Natriuretic Factor, Obesity, Peptide Fragments, Sodium, Receptors, Glucagon, Cross-Over Studies, Natriuretic Peptide, Brain, Endpoint Determination, Glucagon-Like Peptide 1
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