Abstract
Recent experiments in laboratory animals have challenged the conventional view that the dominant effect of CNS noradrenergic neurons in cardiovascular control is sympathetic nervous inhibition and blood pressure reduction, describing instead sympathetic activation. We have tested whether such a stimulant effect on sympathetic outflow is also evident in human hypertension. CNS norepinephrine turnover was estimated from the combined overflow of norepinephrine, MHPG and DHPG into the internal jugular veins. Cerebral blood flow scans allowed differentiation between cortical and subcortical jugular venous drainage.