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Ethanol Counteraction of Clonidine‐Evoked Inhibition of Norepinephrine Release in Rostral Ventrolateral Medulla of Rats
Author(s) -
Mao Limin,
AbdelRahman Abdel A.
Publication year - 1998
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1998.tb03910.x
Subject(s) - clonidine , rostral ventrolateral medulla , chemistry , endocrinology , medicine , norepinephrine , blood pressure , ethanol , hemodynamics , heart rate , anesthesia , dopamine , biochemistry
Previous studies from our laboratory demonstrated an antagonistic hemodynamic interaction between ethanol and clonidine in conscious and in urethane‐anesthetized rats. The present study tested the hypothesis that ethanol produces its effect by counteracting clonidine‐evoked inhibition of norepinephrine (NE) release at its major site of action, the rostral ventrolateral medulla (RVLM). In vivo electrochemical measurement of real‐time changes in NE level in the RVLM of urethane‐anesthetized Sprague‐Dawley rats was made along with blood pressure and heart rate. Clonidine (30 μg/kg, iv) produced significant decreases ( p < 0.05) in NE electrochemical signal and blood pressure. Ethanol (1 g/kg, iv) administered 10 min after clonidine significantly ( p < 0.05) increased NE signal and counteracted clonidine‐evoked hypotension. Equal volume of saline had no effect on NE signal in the RVLM nor on the hypotensive response to clonidine. Pretreatment with the same dose of ethanol (1 g/kg) caused slight increases in RVLM NE level and in blood pressure, but did not influence the electrochemical and blood pressure responses to clonidine; clonidine (30 μg/kg) administration 10 min after ethanol resulted in significant ( p < 0.05) decreases in NE signal and blood pressure. These findings suggest that: (i) ethanol counteraction of the hypotensive action of clonidine involves, at least in part, opposite effects on central pathways that use NE as a neurotransmitter; (ii) the RVLM represents a possible site for the adverse hemodynamic interaction between ethanol and clonidine; and (iii) ethanol‐evoked increase in RVLM NE, which correlates with its pressor effect, is much enhanced when RVLM NE level is reduced by clonidine.