Ethanol effects

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Ethanol effects

The mechanisms of ethanol’s pharmacological and physiological effects on cells, the brain, and the behavior of animals are not fully understood. The nown mechanisms of various pathological and metabolic effects of ethanol are  HYPERLINK "" \t "_blank" hyperlipemia (with the rise inHDL),  HYPERLINK "" \t "_blank" hyperuricemia, the role of acetaldehyde toxicity and alcohol-induced oxidative stress.

Ethanol has diverse effects at relevant concentrations yet also exhibits remarkable specificity on various receptors and ion channels. A potential explanation of the diversity and specificity of ethanol action lies in its ability to modulate various cell signaling proteins, including kinases and phosphatases. These proteins then alter receptor or channel function via alterations in phosphorylation state or alterations in trafficking as well as direct the activity of intracellular signaling cascades.

Ethanol acts as a general nervous system depressant. This effect is at least partially mediated by ethanol's actions on ligand-gated channels to depress overall synaptic activity in the nervous system. Ethanol is generally thought to inhibit excitatory transmission and increase inhibitory transmission via its modulation of neurotransmitter receptor-mediated currents. Inhibitory synaptic transmission is mediated by two neurotransmitters, GABA and glycine. Currents mediated by both GABA and glycine neurotransmitter receptors are modulated by ethanol. Ethanol typically potentiates glycine-activated currents in cultured cells, although ethanol has also been shown to inhibit glycinergic current in some cultured rat ventral tegmental neurons. Ethanol's effects on GABAergic currents are characteristically variable and depend on many factors including cell type, dose of ethanol, and method of ethanol application.

Some recent studies have explored novel mechanisms of ethanol on atherogenesis via effects on HDL composition and function. Other studies have focused on changes in levels of LDL cholesterol (LDL-C), triglyceride, and other factors such as inflammatory markers C-reactive protein (CRP) and lipoprotein-associated phospholipase A2(LpPLA2).

The acute in vivo cardiovascular response to moderate levels of ethanol intake involves sympathetic activation, probably due to peripheral vasodilation, and usually results in an increase in heart rate and maintained or elevated cardiac output. In experimental situations where sympathetic or autonomic blockade is applied, it has been demonstrated both in vivo and in vitro that ethanol reduces myocardial contractility independent of neural influence. Studies on isolated cardiomyocytes from a number of species have confirmed that acute ethanol treatment has a direct negative inotropic effect, which cannot be attributed to the release of secondary mediators by other cell types