. Low-frequency oscillation of sympathetic nerve activity decreases during development of tiltinduced syncope preceding sympathetic withdrawal and bradycardia. Am J Physiol Heart Circ Physiol 289: H1758 -H1769, 2005. First published June 2, 2005; doi:10.1152/ajpheart.01027.2004.-Sympathetic activation during orthostatic stress is accompanied by a marked increase in low-frequency (LF, ϳ0.1-Hz) oscillation of sympathetic nerve activity (SNA) when arterial pressure (AP) is well maintained. However, LF oscillation of SNA during development of orthostatic neurally mediated syncope remains unknown. Ten healthy subjects who developed head-up tilt (HUT)-induced syncope and 10 agematched nonsyncopal controls were studied. Nonstationary timedependent changes in calf muscle SNA (MSNA, microneurography), R-R interval, and AP (finger photoplethysmography) variability during a 15-min 60°HUT test were assessed using complex demodulation. In both groups, HUT during the first 5 min increased heart rate, magnitude of MSNA, LF and respiratory high-frequency (HF) amplitudes of MSNA variability, and LF and HF amplitudes of AP variability but decreased HF amplitude of R-R interval variability (index of cardiac vagal nerve activity). In the nonsyncopal group, these changes were sustained throughout HUT. In the syncopal group, systolic AP decreased from 100 to 60 s before onset of syncope; LF amplitude of MSNA variability decreased, whereas magnitude of MSNA and LF amplitude of AP variability remained elevated. From 60 s before onset of syncope, MSNA and heart rate decreased, index of cardiac vagal nerve activity increased, and AP further decreased to the level at syncope. LF oscillation of MSNA variability decreased during development of orthostatic neurally mediated syncope, preceding sympathetic withdrawal, bradycardia, and severe hypotension, to the level at syncope. autonomic nervous system; baroreflex; blood pressure; heart rate variability; hemodynamics HUMANS HAVE BEEN SUBJECTED to ceaseless orthostatic stresses since they first evolved and assume an orthostatic posture for most of their lives. During standing, gravitational fluid shift toward the lower part of body (i.e., abdominal vascular bed and lower limbs) would cause severe orthostatic hypotension if it were not countered by compensatory mechanisms (23). Orthostatic sympathetic activation has a crucial role in preventing orthostatic hypotension and maintaining arterial blood pressure (AP) (23). Recent studies have reported that orthostatic sympathetic activation is accompanied by an increase in lowfrequency (LF, ϳ0.1-Hz) oscillation of sympathetic nerve activity (SNA) (1, 5). Tilt maneuvers of 75°and 80°greatly increase the LF oscillatory patterns of muscle SNA (MSNA), which mirrored similar changes in LF oscillation of AP (1, 5). However, LF oscillation of SNA has been investigated only in the steady-state orthostatic condition, when AP remains well maintained. It remains unclear whether LF oscillation of SNA changes during development of orthostatic neurally mediated s...

Despite accumulated knowledge on human baroreflex control of muscle sympathetic nerve activity (SNA), whether baroreflex control of muscle SNA parallels that of other SNAs, in particular renal and cardiac SNAs, remains unclear. Using urethane and ␣-chloralose-anesthetized, vagotomized and aortic-denervated rabbits (n ϭ 10), we recorded muscle SNA from tibial nerve by microneurography, simultaneously with renal and cardiac SNAs by wire electrode. To produce a baroreflex open-loop condition, we isolated the carotid sinuses from systemic circulation and altered the intracarotid sinus pressure (CSP) according to a binary white noise sequence of operating pressure Ϯ 20 mmHg (for investigating dynamic characteristics of baroreflex) or in stepwise 20-mmHg increments from 40 to 160 mmHg (for investigating static characteristics of baroreflex). Dynamic high-pass characteristics of baroreflex control of muscle SNA, assessed by the increasing slope of transfer gain, showed that more rapid change of arterial pressure resulted in greater response of muscle SNA to pressure change and that these characteristics were similar to cardiac SNA but greater than renal SNA. However, numerical simulation based on the transfer function shows that the differences in dynamic baroreflex control at various organs result in detectable differences among SNAs only when CSP changes at unphysiologically high rates (i.e., 5 mmHg/s). On the other hand, static reverse-sigmoid characteristics of baroreflex control of muscle SNA agreed well with those of renal or cardiac SNAs. In conclusion, dynamic-linear and static-nonlinear baroreflex control of muscle SNA is similar to that of renal and cardiac SNAs under physiological pressure change.

Since humans are under ceaseless orthostatic stress, the mechanism to maintain arterial pressure (AP) under orthostatic stress against gravitational fluid shift is of great importance. We hypothesized that (1) orthostatic stress resets the arterial baroreflex control of sympathetic nerve activity (SNA) to a higher SNA, and (2) resetting of the arterial baroreflex contributes to preventing postural hypotension. Renal SNA and AP were recorded in eight anaesthetized, vagotomized and aortic-denervated rabbits. Isolated intracarotid sinus pressure (CSP) was increased stepwise from 40 to 160 mmHg with increments of 20 mmHg (60 s for each CSP level) while the animal was placed supine and at 60 deg upright tilt. Upright tilt shifted the CSP-SNA relationship (the baroreflex neural arc) to a higher SNA, shifted the SNA-AP relationship (the baroreflex peripheral arc) to a lower AP, and consequently moved the operating point to marked high SNA while maintaining AP. A simulation study suggests that resetting in the neural arc would double the orthostatic activation of SNA and increase the operating AP in upright tilt by 10 mmHg, compared with the absence of resetting. In addition, upright tilt did not change the CSP-AP relationship (the baroreflex total arc). A simulation study suggests that although a downward shift of the peripheral arc could shift the total arc downward, resetting in the neural arc would compensate this fall and prevent the total arc from shifting downward to a lower AP. In conclusion, upright tilt increases SNA by resetting the baroreflex neural arc. This resetting may compensate for the reduced pressor responses to SNA in the peripheral cardiovascular system and contribute to preventing postural hypotension.

Although electroacupuncture reduces sympathetic nerve activity (SNA) and arterial pressure (AP), the effects of electroacupuncture on the arterial baroreflex remain to be systematically analyzed. We investigated the effects of electroacupuncture of Zusanli on the arterial baroreflex using an equilibrium diagram comprised of neural and peripheral arcs. In anesthetized, vagotomized, and aortic-denervated rabbits, we isolated carotid sinuses and changed intra-carotid sinus pressure (CSP) from 40 to 160 mmHg in increments of 20 mmHg/min while recording cardiac SNA and AP. Electroacupuncture of Zusanli was applied with a pulse duration of 5 ms and a frequency of 1 Hz. An electric current 10 times the minimal threshold current required for visible muscle twitches was used and was determined to be 4.8 Ϯ 0.3 mA. Electroacupuncture for 8 min decreased SNA and AP (n ϭ 6). It shifted the neural arc (i.e., CSP-SNA relationship) to lower SNA but did not affect the peripheral arc (i.e., SNA-AP relationship) (n ϭ 8). SNA and AP at the closed-loop operating point, determined by the intersection of the neural and peripheral arcs, decreased from 100 Ϯ 4 to 80 Ϯ 9 arbitrary units and from 108 Ϯ 9 to 99 Ϯ 8 mmHg (each P Ͻ 0.005), respectively. Peroneal denervation eliminated the shift of neural arc by electroacupuncture (n ϭ 6). Decreasing the pulse duration to Ͻ2.5 ms eliminated the effects of SNA and AP reduction. In conclusion, short-term electroacupuncture resets the neural arc to lower SNA, which moves the operating point toward lower AP and SNA under baroreflex closed-loop conditions. arterial pressure; equilibrium diagram ALTHOUGH THERE ARE MANY clinical case reports (21,30,32,39,40,42), the effects of electroacupuncture on cardiovascular regulation remain to be systematically investigated. There has been a recent renewal of interest in the inhibitory effects of electroacupuncture of the Zusanli acupoint on the cardiovascular system, including reductions in arterial pressure (AP), heart rate, (3,15,16), and sympathetic nerve activity (SNA) (25,42). Such inhibitory effects are observed during lowfrequency (Ͻ20 Hz) electroacupuncture. Because the arterial baroreflex is one of the most important control systems that stabilize AP, we quantified the effects of electroacupuncture on the arterial baroreflex over an entire operating range. Systematic analysis would help to assess the possible utility of electroacupuncture as a treatment modality for certain cardiovascular diseases with vagolytic and sympathotonic states (26,38).One of the best ways to quantitatively analyze changes in the arterial baroreflex over an entire operating range may be analysis using a baroreflex equilibrium diagram (10, 23, 31) (see APPENDIX for details). Briefly, the baroreflex equilibrium diagram consists of a neural arc representing SNA as a function of baroreceptor input pressure and a peripheral arc representing AP as a function of SNA. The intersection of the two arcs corresponds to an operating point of the AP regulation under baroreflex closed-loo...

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