Sympathetic transients caused by abrupt alterations of carotid baroreceptor activity in humans

1982 ◽  
Vol 242 (2) ◽  
pp. H185-H190 ◽  
Author(s):  
B. G. Wallin ◽  
D. L. Eckberg

We examined the role of carotid baroreceptors in the short-term modulation of sympathetic outflow to the muscle vascular bed and parasympathetic outflow to the heart in 10 healthy adults. Afferent carotid baroreceptor activity was modified with 30-mmHg neck suction or pressure applied during held expiration, and efferent sympathetic activity was measured with microelectrodes inserted percutaneously into peroneal nerve muscle fascicles. Sympathetic responses were conditioned importantly by directional changes of carotid transmural pressure: increased pressure (onset of neck suction or offset of neck pressure) inhibited (totally) sympathetic activity, and reduced pressure (offset of neck suction or onset of neck pressure) augmented sympathetic activity. Responses occurred after a latency of about 2 s and did not persist as long as changes of neck-chamber pressure. Cardiac intervals were prolonged by increased carotid transmural pressures and shortened by decreased carotid transmural pressures, but, in contrast to sympathetic responses, cardiac responses adapted only slightly during neck-chamber pressure changes. Our results suggest that in the human a common baroreceptor input is processed differently in central vagal and sympathetic networks. Muscle sympathetic responses to changing levels of afferent baroreceptor traffic are profound but transitory. They appear to be conditioned more by changes of arterial pressure than by its absolute levels.

1987 ◽  
Vol 63 (6) ◽  
pp. 2325-2330 ◽  
Author(s):  
D. L. Eckberg ◽  
B. G. Wallin

The influence of brief, moderate isometric exercise on the earliest vagal and sympathetic responses to changes of afferent carotid baroreceptor activity was studied in 10 healthy young men and women. Vagal-cardiac nerve activity was estimated from changes of electrocardiographic R-R intervals, and postganglionic peroneal nerve muscle sympathetic activity was measured directly from microneurographic recordings. Carotid baroreceptor activity was altered with 5-s periods of 30 Torr pressure or suction applied to a neck chamber during held expiration. Brief handgrip (30% of maximum) significantly reduced base-line R-R intervals, did not modify reductions of R-R intervals during neck pressure, and significantly reduced increases of R-R intervals during neck suction. Handgrip did not significantly increase base-line sympathetic activity from resting levels, but it significantly diminished increases of sympathetic activity during neck pressure and augmented reductions of sympathetic activity during neck suction. Our results suggest that exercise modifies, in small but significant ways, early sympathetic and vagal responses to abrupt changes of arterial baroreceptor input in humans.


1976 ◽  
Vol 51 (s3) ◽  
pp. 347s-349s ◽  
Author(s):  
J. Ludbrook ◽  
G. Mancia ◽  
A. Ferrari ◽  
A. Zanchetti

1. Transmission of pneumatic pressure from a neck chamber to the region of the carotid sinus is imperfect and asymmetric (86% of positive pressure, 64% of negative pressure). This has to be taken into account in the correct analysis of the carotid baroreceptor reflex. 2. There is no evidence for a reduction in cerebral blood flow nor of carotid chemoreceptor stimulation in response to an increase in neck chamber pressure of about 45 mmHg. Thus it is likely that the pressor response to this manoeuvre is in fact due to reduction in carotid baroreceptor activity.


1992 ◽  
Vol 263 (1) ◽  
pp. R215-R220 ◽  
Author(s):  
D. L. Eckberg ◽  
V. A. Convertino ◽  
J. M. Fritsch ◽  
D. F. Doerr

Published information on the reproducibility of human baroreflex responses in the absence of interventions is limited. Therefore, we analyzed retrospectively vagally mediated carotid baroreceptor-cardiac reflex responses of 34 healthy young adult volunteers whom we studied twice, 7-10 days apart (all 34 subjects) or 10 wk apart (8 subjects). We delivered a sequence of neck pressure changes during held expiration: A computer-driven bellows initially raised pressure to approximately 40 mmHg for five heart beats, and then reduced pressure in a stepwise series of R-wave-triggered 15-mmHg decrements to about -65 mmHg. R-R interval changes were plotted as functions of the carotid distending (systolic less neck) pressure occurring within each interval. Each experimental session yielded one stimulus-response relation, which comprised the average of seven separate trials. Six measures were derived from these relations: minimum, maximum, and range of R-R intervals; maximum slope; and operational point [(R-R interval shortening/R-R interval range) x 100%]. Linear regression correlation coefficients for measurements made on two occasions were all highly significant (range: 0.64-0.99). Our results indicate that human vagally mediated carotid baroreceptor-cardiac reflex responses, studied serially under exacting experimental conditions, are highly reproducible.


1987 ◽  
Vol 252 (4) ◽  
pp. R732-R736 ◽  
Author(s):  
G. A. Kasting ◽  
D. L. Eckberg ◽  
J. M. Fritsch ◽  
C. L. Birkett

Although human baroreflex responses have been studied during night as well as day, there has been no attempt to distinguish circadian changes of baroreflex function from those related to sleep. We measured carotid baroreceptor-cardiac reflex responses serially during a 24-h period in 11 normotensive volunteers who were awake and cooperative during testing. We applied sequences of ramped R-wave-triggered neck chamber pressure changes from +40 to -65 mmHg, during held expiration, at 3-h intervals. Subjects maintained their usual sleep-wake cycles but were awakened for three 30-min periods for night testing. There was no systematic change of baroreflex slope during the 24-h period. There were, however, parallel shifts of the entire sigmoid baroreceptor-cardiac reflex response relation along its R-R interval and arterial pressure axes associated with small, but significant, circadian changes of baseline R-R intervals and arterial pressures. Thus, although our data do not point toward major circadian variability of baro-reflex responsiveness, they provide evidence for an ongoing process of human baroreflex resetting.


1986 ◽  
Vol 60 (2) ◽  
pp. 727-732 ◽  
Author(s):  
J. M. Sprenkle ◽  
D. L. Eckberg ◽  
R. L. Goble ◽  
J. J. Schelhorn ◽  
H. C. Halliday

We designed, constructed, and evaluated a new device to characterize the human carotid baroreceptor-cardiac reflex response relation rapidly. We designed this system for study of reflex responses of astronauts before, during, and after space travel. The system comprises a new tightly sealing silicone rubber neck chamber, a stepping motor-driven electro-deposited nickel bellows pressure system, capable of delivering sequential R-wave-triggered neck chamber pressure changes between +40 and -65 mmHg, and a microprocessor-based electronics system for control of pressure steps and analysis and display of responses. This new system provokes classic sigmoid baroreceptor-cardiac reflex responses with threshold, linear, and saturation ranges in most human volunteers during one held expiration.


1991 ◽  
Vol 260 (3) ◽  
pp. R635-R641 ◽  
Author(s):  
J. M. Fritsch ◽  
M. L. Smith ◽  
D. T. Simmons ◽  
D. L. Eckberg

We compared baroreflex modulation of human vagal-cardiac and sympathetic muscle activity in healthy volunteers by measuring R-R interval and peroneal nerve responses to a profile of positive and negative (40-65 mmHg) R-wave-triggered neck pressure steps during held expiration. R-R interval responses were sigmoid. Sympathetic activity increased abruptly with 40 mmHg pressure but returned to baseline levels as this pressure was maintained. The first decremental pressure step reduced sympathetic activity to below baseline, and the next three steps inhibited activity. During the final three steps, sympathetic activity increased to baseline, and after the return of neck pressure to ambient levels sympathetic activity increased to the highest levels recorded. Our results suggest that on a second-by-second basis human vagal-cardiac responses are determined simply by the net level of baroreceptor stimulation. Sympathetic muscle responses are determined complexly by the direction of changes (rising or falling) more than absolute arterial pressure levels and importantly by inputs from both carotid and aortic baroreceptors.


1979 ◽  
Vol 57 (s5) ◽  
pp. 165s-167s ◽  
Author(s):  
G. Mancia ◽  
G. Leonetti ◽  
G. B. Picotti ◽  
A. Ferrari ◽  
M. D. Galva ◽  
...  

1. Slight decreases and increases in carotid baroreceptor activity were induced in subjects with essential hypertension by slight alterations in carotid transmural pressure (variable pressure neck-chamber technique) in order to obtain limited increases and reductions in sympathetic adrenergic activity. 2. When sympathetic activity was reflexly increased there was a rise in arterial pressure but no significant increase in plasma catecholamines. Likewise when sympathetic activity was reflexly reduced there was a fall in arterial pressure but no significant reduction in plasma catecholamines. 3. Plasma noradrenaline and adrenaline significantly and markedly increased in the same subjects when sympathetic activity was increased by activation of both arterial and low pressure baroreceptor reflexes with tilting. 4. It is suggested that measurements of catecholamines in systemic plasma may reveal marked degrees of sympathetic activation but may not be a sensitive index of more moderate changes in sympathetic tone.


1983 ◽  
Vol 65 (3) ◽  
pp. 227-235 ◽  
Author(s):  
G. Mancia ◽  
A. Ferrari ◽  
Luisa Gregorini ◽  
G. Leonetti ◽  
G. Parati ◽  
...  

1. Plasma concentrations of noradrenaline and adrenaline were measured radioenzymatically in nine subjects during 4 min pressor and depressor responses (intra-arterial measurements) induced by increasing and reducing sympathetic vasoconstrictor tone via carotid baroreceptor deactivation and stimulation (neck chamber technique). 2. During the pressor response (15 ± 3 mmHg, mean ± se) plasma noradrenaline and adrenaline showed various changes in the different subjects and on average were not significantly increased above control. During the depressor response (−9 ± 2 mmHg) plasma noradrenaline and adrenaline also showed various changes in the subjects and were on average not significantly reduced below control. 3. In contrast the same subjects all showed an increase in noradrenaline and adrenaline (average 76 and 117%) at the fourth minute of a tilting manoeuvre with- a return to pretilting values no more than 4 min after resumption of the supine position. 4. These results suggest that the moderate and/or restricted alterations in sympathetic tone produced by manipulating a single baroreflex, though capable of affecting blood pressure, are not reflected by alterations in plasma catecholamines. To modify these humoral indices significantly, the more drastic or more diffuse alterations in sympathetic activity that may be produced by manipulating low as well as high pressure reflexogenic areas are needed.


1989 ◽  
Vol 256 (2) ◽  
pp. R549-R553 ◽  
Author(s):  
J. M. Fritsch ◽  
R. F. Rea ◽  
D. L. Eckberg

We studied human baroreflex resetting during 25 min of drug-induced arterial pressure changes in 10 healthy volunteers. Average (+/- SE) base-line systolic pressure of 113 +/- 4 fell to 102 +/- 3 during nitroprusside infusions and rose to 135 +/- 6 mmHg during phenylephrine infusions. Average base-line R-R intervals of 932 +/- 37 shortened to 820 +/- 39 during nitroprusside infusions and lengthened to 1,251 +/- 61 ms during phenylephrine infusions. Carotid baroreceptor-cardiac reflex responses were evaluated with a complex series of neck chamber pressure changes, and R-R intervals were plotted as functions of carotid distending pressure. Baroreceptor-cardiac reflex relations shifted on both R-R interval and arterial pressure axes during drug infusions, but there was no significant change of the maximum slope or range of R-R interval responses. The position of baseline R-R intervals on the reflex relation (operational point) changed significantly. Resting R-R intervals were closer to threshold during pressure reductions and closer to saturation for baroreceptor-cardiac responses during pressure elevations. These results document short-term partial resetting of human baroreceptor-cardiac reflex responses as early as 25 min after the onset of arterial pressure changes.


1992 ◽  
Vol 73 (2) ◽  
pp. 664-671 ◽  
Author(s):  
J. M. Fritsch ◽  
J. B. Charles ◽  
B. S. Bennett ◽  
M. M. Jones ◽  
D. L. Eckberg

Orthostatic intolerance is a predictable but poorly understood consequence of space travel. Because arterial baroreceptors modulate abrupt pressure transients, we tested the hypothesis that spaceflight impairs baroreflex mechanisms. We studied vagally mediated carotid baroreceptor-cardiac reflex responses (provoked by neck pressure changes) in the supine position and heart rate and blood pressure in the supine and standing positions in 16 astronauts before and after 4- to 5-day Space Shuttle missions. On landing day, resting R-R intervals and standard deviations, and the slope, range, and position of operational points on the carotid transmural pressure-sinus node response relation were all reduced relative to preflight. Stand tests on landing day revealed two separate groups (one maintained standing arterial pressure better) that were separated by preflight slopes, operational points, and supine and standing R-R intervals and by preflight-to-postflight changes in standing pressures, body weights, and operational points. Our results suggest that short-duration spaceflight leads to significant reductions in vagal control of the sinus node that may contribute to, but do not account completely for, orthostatic intolerance.


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