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Effects of ethanol ingestion on alpha‐adrenoceptor‐mediated circulatory responses in man.
Author(s) -
Eisenhofer G,
Lambie DG,
Johnson RH
Publication year - 1984
Publication title -
british journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.216
H-Index - 146
eISSN - 1365-2125
pISSN - 0306-5251
DOI - 10.1111/j.1365-2125.1984.tb02507.x
Subject(s) - methoxamine , blood pressure , ingestion , ethanol , vasoconstriction , endocrinology , medicine , circulatory system , heart rate , diastole , chemistry , anesthesia , agonist , biochemistry , receptor
The acute effects of ethanol on pressor responses to graded intravenous infusions of noradrenaline (24, 48, 90 ng kg‐1 min‐1) and methoxamine (0.2, 0.4, 0.8, 1.6, 2.0 mg/min, 1 min each) were each investigated in eight normal male subjects. The effects of ethanol on blood pressure, heart rate and plasma catecholamine responses to lower body negative pressure were also examined in six normal male subjects. Each subject acted as his own control by participating twice, once after consumption of ethanol (1.0 ml/kg, 20% v/v, in orange juice) and once after an equivalent volume of orange juice. Ethanol consumption significantly reduced the diastolic blood pressure response to infusion of noradrenaline. This occurred despite a significantly greater increase in plasma noradrenaline concentrations during infusion after ethanol. The systolic and diastolic blood pressure responses to infusion of methoxamine were both significantly reduced after ethanol. During lower body negative pressure, prior consumption of ethanol resulted in a greater fall in systolic blood pressure and a smaller rise in diastolic blood pressure. Plasma noradrenaline responses to lower body negative pressure were significantly increased after ethanol. It is concluded that acute ethanol ingestion depresses alpha‐adrenoceptor‐mediated vasoconstriction, with resulting impairment of blood pressure control.