The sympathetic nervous system (SNS) plays an important role in the regulat
ion of blood pressure homeostasis and cardiac function. Furthermore, the in
creased SNS activity is a predictor of mortality in patients with hypertens
ion, coronary artery disease and congestive heart failure. Experimental dat
a and a few clinical trials suggest that there are important interactions b
etween the main presser systems, i.e. the SNS, the renin-angiotensin system
and the vascular endothelium with the strongest vasoconstrictor, endotheli
n. The main methods for the assessment of SNS activity are described. Cardi
ovascular drugs of different classes interfere differently with the SNS and
the other pressor systems. Pure vasodilators including nitrates, alpha -bl
ockers and dihydropyridine (DHP)-calcium channel blockers increase SNS acti
vity. Finally, central sympatholytics and possibly phenylalkylamine-type ca
lcium channel blockers reduce SNS activity. The effects of angiotensin-II r
eceptor antagonists on SNS activity in humans is not clear; experimental da
ta are discussed in this review. There are important interactions between t
he presser systems under experimental conditions. Recent studies in humans
suggest that an activation of the SNS with pure vasodilators in parallel in
creases plasma endothelin. It can be assumed that, in cardiovascular diseas
es with already enhanced SNS activity, drugs which do not increase SNS acti
vity or even lower it are preferable. Whether this reflects in lower mortal
ity needs to be investigated in intervention trials.