DOPAMINE AND SYMPATHOADRENAL ACTIVITY IN MAN

The sympathetic adrenal (SA) activity can be modulated by dopamine (DA ) through D2 receptors. In man, using D2 antagonists, it has been demo nstrated that endogenous DA plays an inhibitory modulation of the SA s ystem during high degree of SA activation. D2 agonists are able to ind uce a decrease in norepinephrine (NE) release either in vitro or in vi vo. This effect leads, in vivo, to a decrease in blood pressure (BP) a nd to an activation of arterial baroreceptors. Therefore, in vivo, the D2 mediated inhibition of epinephrine (E) release, which is clearly d emonstrated in vitro, is overwhelmed by the baroreceptor-mediated acti vation of the splachnic nerve. As a consequence, the in vivo administr ation of D2 agonists can induce a different effect on the net peripher al sympathetic tone of an organ, depending on the balance between the degree of the baroreceptor-mediated sympathetic activation and the inh ibitory D2-mediated inhibition of NE release at the tissue level. In t he present paper we investigated the in vivo effect of placebo (PL) or acute oral bromocriptine (BC) administration on plasma CA and on the cardiac sympatho-vagal balance of 7 normal volunteers, as assessed by power spectral analysis of heart rate (HR) variability (autoregressive method), either in resting or sitting position. Low frequency (LF) an d high frequency (HF) components, both expressed in normalized units ( nU), and LF/HF ratio were calculated. BC caused a decrease in BP, plas ma NE and no change in HR in resting and sifting position. Plasma E in creased in sitting position. At the heart level, after BC, we observed , during rest, an increase in LF and LF/HF ra tio and a decrease in HF while in sitting position LF did not increase further. These data sho w that BC, while reducing BP through a decrease of plasma NE, increase s LF/HF ratio (sympathetic tone) without any change in heart rate. The se data seem to confirm that BC causes an inhibitory modulation of the SA system acting predominantly at the periphery through D2 presynapti c receptors.