ArticleScientific reports2016
Caffeine intake antagonizes salt sensitive hypertension through improvement of renal sodium handling.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 32 citations in OpenAlex.
- Elucidation of the effects of caffeine consumption on estrous cycle, hematology, and lipid profile of female Wistar rats.Scientific reports · 2025Article
- Caffeine and neonatal acute kidney injury.Pediatric nephrology (Berlin, Germany) · 2024Review
- Metabolic profiling identifies the significance of caffeine metabolism in CKD.Frontiers in bioengineering and biotechnology · 2023Article
- Coffee intake and risk of diabetic nephropathy: a Mendelian randomization study.Frontiers in endocrinology · 2023Article
- Caffeine alleviates acute liver injury by inducing the expression of NEDD4L and deceasing GRP78 level via ubiquitination.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Article
- Caffeine prevents restenosis and inhibits vascular smooth muscle cell proliferation through the induction of autophagy.Autophagy · 2022Article
- Sodium-Glucose Cotransporter 2 Inhibitor Canagliflozin Antagonizes Salt-Sensitive Hypertension Through Modifying Transient Receptor Potential Channels 3 Mediated Vascular Calcium Handling.Journal of the American Heart Association · 2022Article
- Chronic Intake of Energy Drinks and Their Sugar Free Substitution Similarly Promotes Metabolic Syndrome.Nutrients · 2021Article
- The Consumption of Energy Drinks Induces Blood-Brain Barrier Dysfunction in Wild-Type Mice.Frontiers in nutrition · 2021Article
- Chronic Consumption of a Commercial Energy Drink Reduces Blood Pressure in Normotensive Wild-Type Mice.Frontiers in nutrition · 2019Article
- Pu-Erh Tea Relaxes the Thoracic Aorta of Rats by Reducing Intracellular Calcium.Frontiers in pharmacology · 2019Article
- AMP-Activated Protein Kinase (AMPK)-Dependent Regulation of Renal Transport.International journal of molecular sciences · 2018Review
- Measurement of cations, anions, and acetate in serum, urine, cerebrospinal fluid, and tissue by ion chromatography.Physiological reports · 2018Article
- Coffee with High but Not Low Caffeine Content Augments Fluid and Electrolyte Excretion at Rest.Frontiers in nutrition · 2017Article
- Lack of Effects of Metformin and AICAR Chronic Infusion on the Development of Hypertension in Dahl Salt-Sensitive Rats.Frontiers in physiology · 2017Article
- High salt diet and caffeine: food for thought.Journal of thoracic disease · 2016Article
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15 authors at 4 institutions in 2 countries.
Funding
Abstract
High salt intake is a major risk factor for hypertension. Although acute caffeine intake produces moderate diuresis and natriuresis, caffeine increases the blood pressure (BP) through activating sympathetic activity. However, the long-term effects of caffeine on urinary sodium excretion and blood pressure are rarely investigated. Here, we investigated whether chronic caffeine administration antagonizes salt sensitive hypertension by promoting urinary sodium excretion. Dahl salt-sensitive (Dahl-S) rats were fed with high salt diet with or without 0.1% caffeine in drinking water for 15 days. The BP, heart rate and locomotor activity of rats was analyzed and urinary sodium excretion was determined. The renal epithelial Na(+) channel (ENaC) expression and function were measured by in vivo and in vitro experiments. Chronic consumption of caffeine attenuates hypertension induced by high salt without affecting sympathetic nerve activity in Dahl-S rats. The renal α-ENaC expression and ENaC activity of rats decreased after chronic caffeine administration. Caffeine increased phosphorylation of AMPK and decrease α-ENaC expression in cortical collecting duct cells. Inhibiting AMPK abolished the effect of caffeine on α-ENaC. Chronic caffeine intake prevented the development of salt-sensitive hypertension through promoting urinary sodium excretion, which was associated with activation of renal AMPK and inhibition of renal tubular ENaC.
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