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Last Updated: 3 years ago

Possible Interaction: Ethanol and Vasoconstrictor Agents

Research Papers that Mention the Interaction

Ethanol administration induces an increase in vasoactive agents such as endothelin and nitric oxide and oxidative stress.
Nihon Arukoru Yakubutsu Igakkai zasshi = Japanese journal of alcohol studies & drug dependence  •  2001  |  View Paper
Chronic ethanol increases the reactivity of intact microvessels to vasoconstrictors and results in decreased reactivity to vasodilators.
Alcoholism, clinical and experimental research  •  1994  |  View Paper
Although the mechanism of this vasoconstriction is not fully understood, it is hypothesized that high ethanol levels may directly stimulate the synthesis/release of the vasoconstrictor , endothelin1, and also impair the synthesis and release of nitric oxide, a potent vasodilator [9, 10] .
Cerebrovascular Diseases  •  2008  |  View Paper
While the focal perfusion abnormalities to the cortex and basal ganglia could be explained by the profound vasoconstrictor effects of cocaine, the combinational use of multiple substances including cannabis and alcohol may play a contributory role.
Journal of nuclear medicine : official publication, Society of Nuclear Medicine  •  1991  |  View Paper
The combination of ethanol and hyperthermia can lead to a synergistic effect on carotid vasoconstriction.
Life sciences  •  2017  |  View Paper
These findings suggest that increased vascular responsiveness to vasoconstrictor agents is possibly a link factor in the development and maintenance of the progressive hypertension induced by ethanol consumption.
Toxicology and applied pharmacology  •  2014  |  View Paper
These data indicate that gender influences the vasoconstrictive effects elicited by chronic ethanol consumption and suggest that males may be more susceptible to the associated hypertension.
European journal of pharmacology  •  1999  |  View Paper
Increased sinusoidal responsiveness to the vasoconstrictor ET‐1 in vivo may contribute to the increased susceptibility of ethanol‐fed rats to secondary stresses that increase ET‐1 expression, such as endotoxemia. (
Hepatology  •  1995  |  View Paper