We have previously demonstrated that
ethanol depresses baroreflex
bradycardia by potentiating the similar action of endogenous
gamma-aminobutyric acid (
GABA) in the medullary dorsal vagal complex. In the present study we examined the relative contribution of the sympathetic vs. the parasympathetic nervous system and aortic vs. carotid sinus baroreceptors in this effect. Depressor baroreflex responses were elicited in
urethane-anesthetized male Sprague-Dawley rats by i.v. injection of graded bolus doses of
phenylephrine or by electrical stimulation of the aortic nerve at different frequencies.
Methyl-atropine (2 mg/kg i.v.) greatly attenuated, and bilateral cervical
vagotomy completely eliminated,
phenylephrine-induced reflex
bradycardia, whereas
propranolol (1 mg/kg i.v.) caused a moderate decrease in the reflex bradycardic response.
Ethanol (1 g/kg i.v) did not influence the residual reflex
bradycardia after
methyl-atropine, but significantly decreased the residual reflex
bradycardia after
propranolol. Aortic nerve stimulation caused frequency-dependent
hypotension, which was unaffected by
methyl-atropine, and
bradycardia, which was eliminated by
methyl-atropine. Depletion of endogenous
GABA by pretreatment of rats with 3-mercaptopropionate slightly increased the bradycardic response to aortic nerve stimulation and eliminated its susceptibility to inhibition by
ethanol. Acute aortic nerve
denervation moderately reduced the reflex bradycardic response to
phenylephrine, which was no longer sensitive to inhibition by
ethanol. These findings suggest that 1)
ethanol inhibits baroreflex
bradycardia but not
hypotension, 2) the effect of
ethanol is selective regarding both the afferent (aortic vs. carotid baroreceptors) and efferent limbs of the reflex (vagal vs. sympathetic) and 3) the effect of
ethanol is mediated through endogenous
GABA, probably at the level of the dorsal brainstem.