Bromocriptine, a dopamine agonist, is known to lower cardiovascular mortali
ty in L-dopa-treated patients with Parkinson's disease, probably by reducin
g the cardiac sympathetic activity. We aimed at unmasking the central effec
ts of bromocriptine on the heart by power spectrum analysis. Ten healthy su
bjects (aged 31 +/-2 years) in supine and sitting positions were evaluated
after the administration of bromocriptine (2.5 mg) alone and after pharmaco
logical peripheral D-2-like blockade by domperidone (20 mg). We calculated
(autoregressive method) the following: the low-frequency (LF) component (an
index of cardiac sympathetic tone), the high-frequency (HF) component (an
index of cardiac vagal tone), and the LF/HF ratio (in index of cardiac symp
athovagal balance). With subjects in the supine position, bromocriptine alo
ne induced a significant increase in the LF component and the LF/HF ratio,
together with a reduction in norepinephrine plasma levels and blood pressur
e values. These conflicting effects can be explained as the combined result
of direct and indirect (reflex-mediated) actions of bromocriptine in vivo.
No changes in cardiac autonomic drive were observed with subjects in the s
itting position. After domperidone pretreatment, bromocriptine induced a re
duction in the LF component and in the LF/HF ratio. The sitting position ca
used an increase in heart rate and in the LF/HF ratio. We demonstrated both
peripheral and central effects of bromocriptine. In particular, pretreatme
nt with a peripheral antagonist (domperidone) allowed us to unmask the cent
ral effect of bromocriptine on cardiac sympathetic drive.