Evidence map›Paper›PMID 42793100›Full record

ReviewBiomolecules2026

Alcohol and Hypertension-A Fresh Look on the Mechanistic Aspects of a Fatal Epidemiologic Relationship.

Klaus Groschner, Ichiro Wakabayashi

Abstract readReview
In one paragraph

Review in Biomolecules, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Klaus GroschnerDivision of Medical Physics and Biophysics, Gottfried Schatz Research Center, Medical University of Graz, 8010 Graz, Austria.ORCID 0000-0002-8659-377X
Ichiro WakabayashiDepartment of Preventive Medicine, School of Medicine, Hyogo Medical University, Nishinomiya 663-8501, Hyogo, Japan.

Funding

FWF Austrian Science Fund PAT9543223Japan Society for the Promotion of Science 25K13516
6 · The paper itself

Abstract

Arterial hypertension is a key trigger for all major, life-threatening cardiovascular events such as arrhythmia, stroke, cardiac infarction and heart failure. Ethanol consumption has been identified as a critical risk factor, which promotes hypertension and thereby corrupts cardiovascular health and limits overall life expectancy. For heavy drinkers (≥72 g/day), reduction in half of the alcohol consumption reportedly results in considerable decreases in systolic and diastolic blood pressure levels amounting to 5.50 and 3.97 mmHg, respectively. Based on the complex network of ethanol effects on mammalian physiology, diverse mechanistic concepts have been postulated for a causal linkage between alcohol consumption and distorted blood pressure regulation. The impact of ethanol on the cardiovascular system involves a wide range of ethanol-sensitive cell types, ranging from neurons to vascular smooth muscle, endothelial and immune-cells, all of which express an interdependent array of potential ethanol target structures. Here, we provide an update on currently available evidence for a causal link between alcohol consumption and the etiology of arterial hypertension. The potential role of ethanol target structures with particular focus on membrane ion channels is discussed along with novel concepts of lipid-dependent modulation of signaling processes in the plasma membrane by ethanol.

Indexed as

Alcohol DrinkingEthanolHypertensionAnimalsBlood PressureHumansEthanolalcohol associated diseasesarterial hypertensionethanolion channelsprotein–lipid interactions

Identifiers

PMID42793100
PMCPMC13604747

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.