Studies performed in experimental animals and in humans have documente
d that high blood pressure markedly impairs baroreceptor control of he
art rate. Whether a similar impairment also characterizes baroreceptor
control of sympathetic activity modulating peripheral vasomotor tone
is still unknown. In 28 untreated essential hypertensive subjects [14
of moderate and 14 of more severe degree, age 51.6+/-2.4 and 52.6+/-2.
1 years (mean+/-SEM)] and in 13 untreated secondary hypertensives (ren
ovascular or pheochromocytoma, age 50.1+/-4.6 years), we measured beat
-to-beat arterial blood pressure (finger photoplethysmographic device)
, heart rate (electrocardiogram, and efferent postganglionic muscle sy
mpathetic nerve activity (microneurography) at rest and during barorec
eptor stimulation and deactivation induced by stepwise intravenous inf
usions of phenylephrine and nitroprusside, respectively. Data were com
pared with those obtained in 15 age-matched normotensive control subje
cts. Muscle sympathetic nerve activity (bursts per 100 heart beats) sh
owed a progressive and significant (P<.01) increase from normotension
(40.3+/-3.3) to moderate (55.6+/-4.1) and more severe essential hypert
ension (68.2+/-4.1), paralleling the progressive increase in blood pre
ssure values. In contrast, muscle sympathetic nerve activity was not i
ncreased in secondary hypertensives (40.5+/-6.7) despite blood pressur
e values similar to or even greater than those of severe essential hyp
ertensives. In both essential and secondary hypertensives, barorecepto
r-heart rate control was displaced toward elevated blood pressure valu
es and markedly impaired compared with normotensive subjects (average
reduction, 38.5%). In contrast, the sympathoinhibitory and sympathoexc
itatory responses to baroreceptor stimulation and deactivation were di
splaced toward elevated blood pressure values but similar in all group
s. Thus, sympathetic activation characterizes essential but not second
ary hypertension. Regardless of its nature, however, hypertension is n
ot accompanied by an impairment of baroreceptor modulation of sympathe
tic activity.