Our previous studies showed that the ability of ethanol or cholidine to alt
er the baroreflex control of heart rate (baroreflex sensitivity, BRS) depen
ds on the functional activity of aortic baroreflexes. In this study, we inv
estigated the interaction between the two drugs on BRS in conscious rats wi
th intact baroreflexes (shamoperated, SO) and after aortic baroreceptor den
ervation (ABD). The slope of the curve relating increments in mean arterial
pressure induced by phenylephrine to corresponding reflex bradycardic resp
onses was taken as an index of BRS. Ethanol (1 g/kg IV) significantly (p <
0.05) attenuated BRS in SO rats (-1.7 +/- 0.13 versus -1.04 +/- 0.15 beats/
min/mm Hg) but not in ABD rats. Clonidine (30 mu g/kg, IV) elicited signifi
cantly (p < 0.05) greater hypotensive responses in conscious ABD compared w
ith SO rats. The BRS was not affected by clonidine administration in SO rat
s but showed significant (p < 0.05) reductions in ABD rats. Ethanol (1 g/kg
, IV) had no effect on the hypotensive response to subsequently administere
d clonidine in ABD and SO rats; however, the effect of the two drugs on BRS
was variable. In ABD rats, the BRS values before and after administration
of ethanol and clondine were similar, suggesting that pretreatment with eth
anol counteracted clonidine-evoked attenuation of BRS in this rat preparati
on. In SO rats, the ethanol-clonidine combination produced a significant (p
< 0.05) decrease in BRS, similar to the effect of ethanol when administere
d alone. These data confirm earlier findings that the aortic baroreflex are
modulates the interaction of ethanol and clonidine with baroreflex functio
n. Further, the ability of ethanol to abolish clonidine-induced attenuation
of BRS in ABD rats may relate to the compound effects of the two drugs on
neuronal pathways participating in the central processing of baroreflexes i
n these rats. (C) 1999 Elsevier Science Inc. All rights reserved.