The importance of the arterial baroreflex control of muscle sympathetic nerve activity (MSNA) has been investigated in physiological conditions and in cardiovascular dysfunctions. However, there is no consensus about the role played by the MSNA in hypertensive states, probably due to the diversity of the methods used to study the arterial baroreflex control of MSNA. In the present study we evaluated the reflex changes in MSNA by increasing and decreasing the mean arterial pressure (MAP) through 1 min intravenous infusion of phenylephrine (1 microgram/kg) and sodium nitroprusside (1 microgram/kg), respectively, in eight normotensive and eight mild hypertensive subjects. Both MAP and MSNA were significantly higher in hypertensive (117 +/- 2 mm Hg and 30 +/- 3 bursts/min) than in normotensive (96 +/- 4 mm Hg and 20 +/- 3 bursts/min) subjects. The reflex gain was calculated by the ratio percent of changes in MSNA/percent changes in MAP. The maximal reflex gain was statistically similar in normotensive and hypertensive groups during phenylephrine (5.1 +/- .4 v 4.3 +/- 0.4 bursts/mm Hg, respectively) and nitroprusside (10.7 +/- 2.3 v 8.1 +/- 1.3 bursts/mm Hg, respectively) infusion. The present data showing that arterial baroreflex control of MSNA is not depressed in hypertensive subjects indicate that the elevated basal MSNA and the mild hypertension in human beings is not a consequence of baroreflex control of MSNA dysfunction.