The influences of life habits on the cardiovascular system may have important implications for public health, as cardiovascular diseases are among the leading causes of shorter life expectancy worldwide. A link between excessive ethyl alcohol (ethanol) consumption and arterial hypertension was first suggested early last century. Since then, this proposition has received considerable attention. Support for the concept of ethanol as a cause of hypertension derives from several epidemiologic studies demonstrating that in the general population, increased blood pressure is significantly correlated with ethanol consumption. Although the link between ethanol consumption and hypertension is well established, the mechanism through which ethanol increases blood pressure remains elusive. Possible mechanisms underlying ethanol-induced hypertension were proposed based on clinical and experimental observations. These mechanisms include an increase in sympathetic nervous system activity, stimulation of the renin-angiotensin-aldosterone system, an increase of intracellular Ca(2+) in vascular smooth muscle, increased oxidative stress and endothelial dysfunction. The present report reviews the relationship between ethanol intake and hypertension and highlights some mechanisms underlying this response. These issues are of interest for the public health, as ethanol consumption contributes to blood pressure elevation in the population.
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http://dx.doi.org/10.4330/wjc.v6.i5.283 | DOI Listing |
Synapse
January 2025
Department of Science, De La Salle College, Institute of the Brothers of the Christian Schools, Toronto, Ontario, Canada.
Alcohol consumption is known to affect dopamine (DA) release in the brain, with significant implications for understanding addiction and its neurobiological underpinnings. This meta-analysis examined the effects of acute alcohol administration on striatal DA release in healthy humans as measured with [C]-raclopride positron emission tomography (PET). Oral alcohol administration was associated with a significant reduction in [C]-raclopride binding potential (BP) in the ventral striatum (Cohen's d = -0.
View Article and Find Full Text PDFAlcohol
December 2024
Department of Pharmacology, Addiction Science, and Toxicology, University of Tennessee Health Science Center, Memphis, TN, USA. Electronic address:
Introduction: Chronic alcohol exposure in humans and rodents causes tolerance to the analgesic effects of alcohol, and enhances pain sensitivity during alcohol withdrawal (i.e., hyperalgesia).
View Article and Find Full Text PDFActa Crystallogr E Crystallogr Commun
October 2024
The mol-ecule of the title compound, [Ni(CHO)(CHN)(HO)]·CHOH, has triclinic () symmetry. This compound is of inter-est for its anti-microbial properties. The asymmetric unit comprises two independent complex mol-ecules, which are linked by N-H⋯O and O-H⋯O hydrogen bonds along [111].
View Article and Find Full Text PDFPhysiol Behav
December 2024
Molecular and Behavioral Neuroscience Laboratory, Pharmacology Department, Universidade Federal de São Paulo, Brazil.
Alcohol use disorder (AUD) is a condition with multifactorial causes, including biopsychosocial factors. Childhood exposure to stress may increase susceptibility to AUD in adulthood. Despite its significance, the interaction between stress and AUD remains unclear.
View Article and Find Full Text PDFBone
December 2024
Center of Bone Biology, Institute for Anatomy, Faculty of Medicine, Dr Subotica starijeg 4, 11000 Belgrade, Serbia. Electronic address:
Objectives: Alcoholic bone disease has been recognized in contemporary literature as a systemic effect of chronic ethanol consumption. However, evidence about the specific influence of alcoholic liver cirrhosis (ALC) on mandible bone quality is scarce. The aim of this study was to explore microstructural, compositional, cellular, and mechanical properties of the mandible in ALC individuals compared with a healthy control group.
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