Influence of acute alcohol ingestion on sympathetic neural responses to orthostatic stress in humans

Abstract

Acute alcohol consumption is reported to decrease mean arterial pressure (MAP) during orthostatic challenge, a response that may contribute to alcohol-mediated syncope. Muscle sympathetic nerve activity (MSNA) increases during orthostatic stress to help maintain MAP, yet the effects of alcohol on MSNA responses during orthostatic stress have not been determined. We hypothesized that alcohol ingestion would blunt arterial blood pressure and MSNA responses to lower body negative pressure (LBNP). MAP, MSNA, and heart rate (HR) were recorded during progressive LBNP (−5, −10, −15, −20, −30, and −40 mmHg; 3 min/stage) in 30 subjects (age 24 ± 1 yr). After an initial progressive LBNP (pretreatment), subjects consumed either alcohol (0.8 g ethanol/kg body mass; n = 15) or placebo ( n = 15), and progressive LBNP was repeated (posttreatment). Alcohol increased resting HR (59 ± 2 to 65 ± 2 beats/min, P < 0.05), MSNA (13 ± 3 to 19 ± 4 bursts/min, P < 0.05), and MSNA burst latency (1,313 ± 16 to 1,350 ± 17 ms, P < 0.05) compared with placebo (group × treatment interactions, P < 0.05). During progressive LBNP, a pronounced decrease in MAP was observed after alcohol but not placebo (group × time × treatment, P < 0.05). In contrast, MSNA and HR increased during all LBNP protocols, but there were no differences between trials or groups. However, alcohol altered MSNA burst latency response to progressive LBNP. In conclusion, the lack of MSNA adjustment to a larger drop in arterial blood pressure during progressive LBNP, coupled with altered sympathetic burst latency responses, suggests that alcohol blunts MSNA responses to orthostatic stress.

Sympathoexcitation and pressor responses induced by ethanol in the central nucleus of amygdala involves activation of NMDA receptors in rats

“…We conclude that ethanol and acetate increase sympathetic outflow and arterial pressure, which may involve the activation of NMDA receptors in CeA neurons projecting to the RVLM. amygdala; acetate; ethanol; glutamate receptors; sympathetic nerve activity; N-methyl-D-aspartate ALCOHOL CONSUMPTION is able to cause an increase in arterial pressure (AP) and/or sympathetic outflow in both humans (8,19,21,26,37,59) and animals (9,38,39,42,57). Increased secretion of arginine vasopressin (38) and corticotrophin-releasing hormone (37), as well as enhanced vascular reactivity to the vasoconstrictor agent phenylephrine (39, 57), may underlie the mechanisms responsible for the alcohol-induced increased in AP.…”

Cardiovascular and cutaneous responses to the combination of alcohol and soft drinks: the way to orthostatic intolerance?

“…Previous studies already reported impairment of the vasoconstrictor response to orthostatic head up tilt test after alcohol ingestion (Narkiewicz et al, 2000;Carter et al, 2011). In contrast to those authors, we used active standing and a more moderate dose of alcohol (0.4 g.kg −1 of body weight instead of 0.8-1.0 g.kg −1 of body weight).…”

“…Many studies analyzed the acute cardiovascular response to alcohol at relatively moderate doses (0.3-1.0 g.kg −1 body weight) corresponding to social drinking. In healthy normotensive subjects, it is characterized by an increase in heart rate (HR), small early (Iwase et al, 1995), late (Randin et al, 1995) or no changes in blood pressure (BP) (Kupari, 1983;van de Borne et al, 1997;Spaak et al, 2008Spaak et al, , 2010Carter et al, 2011), slightly elevated values of cardiac output (CO) and systemic vasodilation (Kupari, 1983), along with activation of the sympathetic nervous system (Iwase et al, 1995;Randin et al, 1995;van de Borne et al, 1997;Hering et al, 2011) and evidence of some vagal withdrawal (Koskinen et al, 1994;Spaak et al, 2010). Interestingly, alcohol may decrease myocardial contractility in healthy young people (Kelly et al, 1996), already evident at concentrations corresponding to the legal driving limit of 0.5 0 / 00 common in most Western Europe.…”

“…Interestingly, alcohol may decrease myocardial contractility in healthy young people (Kelly et al, 1996), already evident at concentrations corresponding to the legal driving limit of 0.5 0 / 00 common in most Western Europe. In addition, alcohol depresses the vasoconstrictor response to noradrenaline infusion (Eisenhofer et al, 1984) and may interfere with the autonomic nervous system, as it disrupts the vasoconstrictor response to orthostatic stress (Narkiewicz et al, 2000;Carter et al, 2011), and impairs baroreflex function (Abdel-Rahman et al, 1987;Carretta et al, 1988). In this context, it comes to no surprise that alcohol consumption may induce orthostatic hypotension, even in young, healthy subjects.…”

“…Although the effects of acute alcohol consumption have been well studied in healthy individuals, including an orthostatic stress (Narkiewicz et al, 2000;Carter et al, 2011), the interaction of sugary drinks with alcohol on cardiovascular regulation has not been well characterized. In most cardiovascular studies, alcohol is given alone (diluted with water, with some sweetening agent or diluted in some fruit juice).…”