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1 Department of Cardiology/Hypertension Clinic, Erasme Hospital, 1070 Brussels, Belgium; 2 Centro Ricerche Cardiovascolari, Consiglio Nazionale delle Ricerca, Dipartimento di Scienze Precliniche Laboratorio Interdisciplinare Technologie Avanzare di Vialba, Medicina Interna II, Ospedale L. Sacco, Università degli studi di Milano, 20157 Milano, Italy; and 3 Hypertension and Cardiovascular Divisions, Mayo Clinic, Rochester, Minnesota 55902
The relative contributions of a
central neural oscillator and of the delay in 
-adrenergic
transmission within the baroreflex loop in the predominance of
low-frequency (LF) cardiovascular variability during sympathetic
activation in humans are unclear. We measured R-R interval (RR), muscle
sympathetic nerve activity (MSNA), blood pressure (BP), and their
variability in 10 normal subjects during sympathetic activation
achieved by BP lowering with sodium nitroprusside (SNP) and
-adrenergic blockade using phentolamine. SNP and phentolamine
induced comparable reductions in BP (P > 0.25).
Despite tachycardia and sympathetic activation with both SNP and
phentolamine, LF variability in RR, MSNA, and BP increased during SNP
and decreased during phentolamine (SNP: RR +20 ± 6%, MSNA
+3 ± 5%, systolic BP +9 ± 6%, diastolic BP +7 ± 5%; phentolamine: RR 
2 ± 7%, MSNA 34 ± 6%, systolic
BP 16 ± 8%, diastolic BP 13 ± 4%, P < 0.05 except systolic BP, where P = 0.09). Thus LF
variability is reduced when sympathetic activation is induced by
-adrenergic blockade. This suggests that -adrenergic transmission
within the baroreflex loop may contribute importantly to the
predominance of LF cardiovascular variability associated with
sympathetic excitation in humans.
sympathetic nervous system
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