Two sites for modulation of human sympathetic activity by arterial baroreceptors

Human muscle sympathetic activity (MSA) is modulated by arterial baroreflex mechanisms: the sympathetic impulses are grouped in pulse synchronous bursts occurring preferentially during transient reductions of blood pressure (Delius et al. 1972), and changes in arterial baroreceptor firing induce reciprocal changes in the strength of the MSA (Wallin et al. 1975; Wallin & Eckberg, 1982). In each subject an approximately constant baroreflex latency can be defined, i.e. a given sympathetic burst can always be related to a given cardiac cycle (Delius et al. 1972). This basic relationship is similar in all subjects despite the fact that some subjects have few, and others many, sympathetic bursts. Such interindividual differences in the amount of activity are highly reproducible over several years (Sundlof & Wallin, 1977; Fagius & Wallin, 1993). Different methods have been used to quantify the arterial baroreflex influence on MSA. In an early study, Sundlof & Wallin (1978) described the relationship between spontaneous variations of blood pressure and nerve traffic in terms of (1) threshold (i.e. whether or not a sympathetic burst is generated) and (2) baroreflex sensitivity (i.e. the slope of the relationship between the strength of a burst and the diastolic pressure in the corresponding heart beat). The same approach has been used to study baroreflex sensitivity during sleep (Nakazato et al. 1998) and to compare groups of normotensive and hypertensive subjects (Wallin & Sundlof, 1979). More commonly, baroreflex effects on MSA have been quantified by measuring the relationship between changes in MSA and blood pressure induced by injections of vasoactive drugs. This approach has been used to study baroreflex sensitivity in healthy subjects at different ages (e.g. Ebert et al. 1992; Matsukawa et al. 1996), in association with manoeuvres (e.g. Halliwill et al. 1996), in cardiovascular diseases (e.g. Ferguson et al. 1992; Grassi et al. 1995; Carlson et al. 1996; Meyrelles et al. 1997) or after administration of anaesthetic drugs (e.g. Sellgren et al. 1994; Muzi & Ebert, 1995). Surprisingly, neither method has been used to quantify arterial baroreflex characteristics in individual subjects. Thus, it is not known whether significant arterial baroreflex thresholds and sensitivites in MSA can be defined for all subjects, and whether, in a given subject, such measures of arterial baroreflex function are reproducible. It is also unknown whether baroreflex characteristics in MSA differ between subjects with few and many MSA bursts at rest. The aim of the present study was to answer these questions. Baroreflex threshold and sensitivity were determined from spontaneous variations of blood pressure/cardiac interval and sympathetic nerve traffic (Sundlof & Wallin, 1978). To minimize random variations in the results, a study of the method of analysis was also included.