Abstract-Although the  1 -adrenergic blocking agent atenolol is an established antihypertensive therapy, its effect on peripheral sympathetic vasoconstrictor drive has remained controversial. In patients with hypertension, atenolol therapy has been reported to either increase or have no effect on peripheral vascular resistance, despite other reports showing no change or a decrease in peripheral sympathetic drive. This study was designed, in patients with untreated essential hypertension (EHT), to quantify changes in simultaneously measured peroneal muscle sympathetic nerve activity (MSNA) and calf vascular resistance (CVR) accompanying atenolol therapy. MSNA was quantified as the mean frequency of single units (s-MSNA) and as multiunit bursts (MSNA bursts) using the technique of microneurography, and CVR was measured using a standard plethysmographic technique. Firstly, by comparing two age-and body weightmatched groups, each of 14 patients with hypertension, we found that the group on atenolol therapy (treated-HT) had similar MSNA values counted over the same number of cardiac beats and similar CVR levels (at least PϾ0.40) to the group without therapy (untreated-HT). Secondly, we examined 10 EHT patients before and after 8Ϯ0.4 weeks of oral atenolol therapy (HT-A) in comparison to seven control patients with hypertension and no treatment (HT-C) who were examined over a similar period of time. We found that the measures of MSNA and CVR did not significantly change in both groups. We conclude that the arterial pressure lowering effect of atenolol was not related to significant changes in central vasoconstrictor sympathetic drive to the periphery. Key Words: antihypertensive therapy Ⅲ sympathetic nervous system Ⅲ hypertension, essential Ⅲ vascular resistance A lthough -adrenergic blocking agents are widely used to lower arterial pressure in essential hypertension (EHT), the mechanisms underlying this effect are not entirely clear. [1][2][3][4] In the case of cardioselective  1 -adrenoceptor antagonists, there has been controversy as to whether or not their arterial pressure lowering effect involves changes to peripheral sympathetic vasoconstrictor drive and hence vascular resistance. For instance, in patients with EHT, atenolol therapy that produced a reduction in arterial pressure and heart rate has been found either to have no effect on forearm and calf vascular resistance or to increase it. 5-9 Similar results have been reported using metoprolol, another  1 -adrenoceptor antagonist. 6,10 -12 Furthermore, in patients with hypertension treated with  1 -adrenoceptor antagonists, reports of an effect on peripheral sympathetic drive mediating the arterial pressure reduction have also been inconsistent. For example, atenolol therapy has been reported to have no effect on biomedical indicators of sympathetic activity such as plasma norepinephrine levels or total body norepinephrine spillover rates. 9,13,14 Even direct measurements of muscle sympathetic nerve activity (MSNA) by peroneal microneurography have bee...