Impairment of baroreceptor reflex control of heart rate but not sympathetic efferent discharge by central neuroadministration of ethanol.

Abstract

We investigated the acute hemodynamic effects of ethanol microinjection into brain areas known to influence cardiovascular function and reflexes. In chloralose-anesthetized rats, ethanol had no effect on baseline mean arterial pressure, heart rate, or sympathetic efferent discharge when microinjected into the nucleus tractus solitarius, the dorsal motor nucleus of the vagus, the rostral ventrolateral medulla, or the posterior hypothalamus. On the other hand, ethanol microinjection into the anterior hypothalamus caused a site-dependent pressor effect and an increase in sympathetic efferent discharge. Baroreceptor heart rate response but not sympathetic efferent discharge response was impaired by ethanol microinjection into the nucleus tractus solitarius, the dorsal motor nucleus of the vagus, and the rostral ventrolateral medulla, suggesting that ethanol involves one or more of these areas in its inhibitory effect on baroreceptor heart rate response and that ethanol has a selective action on baroreceptor reflex control of heart rate. The findings that 1) the effect was dose dependent and 2) injection of ethanol outside of, or an equal volume of cerebrospinal fluid into, the nucleus tractus solitarius had no effect on the response strongly suggest that the observed effect on baroreceptor heart rate response was ethanol mediated. Ethanol microinjection into the dorsal motor nucleus of the vagus impaired the heart rate response, thus raising the possibility that leakage of ethanol to that area from the nucleus tractus solitarius might have contributed to its effect. These findings show that ethanol has a pressor and sympathoexcitatory site of action within the anterior hypothalamus and that it selectively impairs baroreceptor heart rate response via a central site of action; the mechanisms by which ethanol produces these effects remain to be elucidated.

Mechanics of the carotid artery wall and baroreflex sensitivity after acute ethanol administration in young healthy volunteers

“…Obviously, carotid vasodilatation, like the forearm vasodilatation reported previously [28], could be caused by factors other than haemodynamic compensatory mechanisms, such as central modulation of vasomotor tone [9], a direct effect of ethanol on the vessel wall [15], α-receptor blockade [16], or interference with transmembrane ion transport [17] and\or with substances released from the endothelium [18]. Among these hypotheses, interference with the central nervous system seems the most unlikely under our experimental conditions, since the dose of alcohol that we used was very small ; heart rate, as an index of autonomic nervous system activity, showed only insignificant changes after alcohol consumption.…”

“…In addition, alcohol administration could have attenuated the baroreceptor heart rate response by interfering with the central regulation of the reflex or by a direct action on the heart through the well-known depressive effects of ethanol in these two organs [2,[9][10][11][12]. However, these effects are dose-dependent, and slight or absent at the dose we used in the present study [2,14].…”

“…Alcohol could potentially interfere with each component of the baroreflex control of heart rate : the peripheral receptors at aortic and carotid sites, central nervous regulation, and the heart directly. It is well known that ethanol is capable of modifying vessel diameter [8], of interacting with the central [9] and autonomic [10] nervous systems, and of impairing cardiac function [11][12][13]. These last two effects are dose-dependent [14].…”

Suppression of Alcohol-Induced Hypertension by Dexamethasone

“…9 Our results provide some mechanistic insight into alcohol-induced sympathetic activation. In rats, alcohol stimulates CRH release 13,14 ; both alcohol 12 and CRH 18 exert sympathoexcitatory and pressor effects when administered centrally; and dexamethasone, presumably by inhibiting CRH release, attenuates stress-induced sympathetic activation. 18 In this study of humans, dexamethasone impaired the ability of alcohol to stimulate the discharge of sympathetic nerves.…”

“…[9][10][11] Moreover, in rats the alcohol-induced increases in blood pressure and sympathetic activity are centrally mediated. 12 Alcohol stimulates the secretion of corticotropinreleasing hormone (CRH) in rats, 13,14 an effect that could explain why regular alcohol consumption stimulates cortisol secretion. 15 In rats, the intracerebroventricular administration of CRH increases blood pressure 16 and stimulates sympathetic activity, 17 and the inhibition of CRH release by dexamethasone attenuates stress-induced sympathetic activation.…”