Our previous studies showed that the hypotensive effect of
clonidine is enhanced in rats with surgically eliminated aortic baroafferents. In this study, we investigated whether this effect of
clonidine is related to facilitation of baroreceptor control of reflex
bradycardia. The effects of
clonidine on blood pressure (BP), heart rate (HR), and baroreflex-mediated decreases in HR (baroreflex sensitivity, BRS) were studied in conscious aortic barodenervated (ABD) and
sham-operated (SO) rats. The slope of the baroreflex curve relating increments in mean arterial pressure (MAP) induced by
phenylephrine to corresponding baroreflex-mediated bradycardic responses was taken as an index of BRS. ABD but not the
sham operation caused immediate and significant (p < 0.05) increases in BP and HR and an impairment of BRS. Two days after ABD, these parameters, except the BRS, subsided to near control levels. Starting from similar baseline values of BP and HR,
clonidine (30 microg/kg, i.v.) elicited significantly (p < 0.05) greater decreases in MAP in conscious ABD rats compared with SO rats (-23 +/- 2 mm Hg vs. -7 +/- 2 mm Hg). The enhanced hypotensive effect of
clonidine in ABD rats was associated with a significant reduction in baroreceptor-mediated reflex bradycardic responses to increments in BP evoked by
phenylephrine. The slope of the baroreflex curves that represented the BRS showed approximately 40% reduction
after treatment with
clonidine (baseline BRS, -1.2 +/- 0.06 beats/min/mm Hg;
clonidine, -0.73 +/- 0.07 beats/min/mm Hg). On the other hand, a threefold lower decrease in BP by
clonidine in SO rats was not associated with any alteration in BRS. These findings support the hypothesis that aortic baroreceptors exert a tonically active restraining influence on centrally mediated
hypotension. More important, the results do not favor a role for facilitation of baroreflexes in the enhanced hypotensive effect of
clonidine in denervated rats.