(Hypertension. 1996;27:442-448.)
© 1996 American Heart Association, Inc.
Articles |
Acute Baroreflex Resetting
Differential Control of Pressure and Nerve Activity
From the Zablocki Department of Veterans Affairs Medical Center and Departments of Anesthesiology and Physiology, The Medical College of Wisconsin, Milwaukee.
Correspondence to Heather A. Drummond, PhD, Medical College of Wisconsin, Milwaukee, WI 53226. E-mail hdrummon@post.its.mcw.edu.
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Abstract |
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Abstract This study evaluated acute resetting of carotid baroreflex control of arterial blood pressure and renal or thoracic sympathetic nerve activity in thiopental-anesthetized mongrel dogs with the use of a vascularly isolated carotid sinus preparation, the experimental model used previously to characterize acute resetting in carotid baroreceptor afferent fibers. Carotid baroreceptors were conditioned with a pulsatile pressure for 20 minutes at three pressure ranges: low (50 to 75 mm Hg), mid (100 to 125), or high (150 to 175). Blood pressure and nerve activity were recorded in response to slow ramp increases in sinus pressure; nonlinear regression and best-fit analyses were used for determination of curve fit parameters of the blood pressure and nerve activity versus sinus pressure response curves. Carotid sinus pressure thresholds for blood pressure and renal nerve activity responses at all conditioning pressures were significantly different; however, only the pressure threshold for thoracic nerve activity at the low conditioning pressure was significantly different from the responses at other conditioning pressures. Average renal activity resetting (0.506±0.072) was significantly greater than blood pressure resetting (0.335±0.046) in the same dogs, and thoracic activity (0.200±0.057) was not different from blood pressure resetting (0.194±0.031) in the same dogs. In a previous investigation, our laboratory has demonstrated that type 1 carotid baroreceptors acutely reset at a value of about 0.15. These results indicate that (1) renal and thoracic nerve activities and blood pressure acutely reset to a greater degree than type 1 carotid baroreceptors and that (2) renal activity acutely resets to a greater degree than blood pressure and thoracic nerve activity.
Key Words: carotid sinus • sympathetic nerve activity • thoracic nerves • pressoreceptors
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Introduction |
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TopAbstractIntroductionMethods Results Discussion References |
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Acute resetting of arterial baroreceptors1 2 3 and the arterial baroreflex4 5 6 7 8 9 has been clearly demonstrated. Within 5 to 30 minutes after the baroreceptors are exposed to a change in CP, the baroreceptor stimulus (pressure)–response (baroreceptor activity) curve will shift in the direction of the pressure change, producing a shift in the Pth of the reflex.3 10 11 The extent of resetting is determined by comparison of the change in Pth with the change in CP: Fraction of Resetting=
Pth/CP. Previously, our laboratory
determined that type 1 carotid baroreceptors reset at a
value of 0.12 to 0.15 within 25 minutes, whereas type 2 carotid
baroreceptors did not acutely reset.1 Although other
researchers3 12 have reported similar findings,
Munch11 reported that acute resetting in rat aortic
baroreceptors with discharge patterns similar to those of the type 1
and 2 carotid baroreceptors was similar. Although rabbit carotid
baroreceptors with both myelinated and
unmyelinated afferents reset, baroreceptors with
myelinated afferents reset to a greater extent than
baroreceptors with unmyelinated
afferents.10 With the use of different experimental models with different methodologies, investigations on acute baroreflex resetting control of arterial BP and SNA have reported a wide range of resetting values, from 0.15 to 0.80.4 6 8 13 14 15 16 Reports on acute carotid baroreflex resetting in bilaterally isolated carotid sinus preparations in the dog, which is similar to the unilateral isolated carotid sinus preparation in the present investigation, have reported acute resetting in the range of 0.15 to 0.60.6 8 14 15 16 Although acute resetting of baroreflex control of regional SNA was not reported in these investigations, only a few studies have simultaneously evaluated reflex control of BP and regional SNA. In anesthetized rabbits, Heesch and Barron5 found that a 10-minute electrical stimulation of the aortic nerve produced a significant increase in the midpoint of the reflex curve for BP but not for lumbar SNA, suggesting that BP but not lumbar SNA resets. Kunze7 reported prolonged inhibition of RSNA compared with BP after aortic nerve stimulation in sinodenervated rabbits. Kunze also reported that after aortic nerve stimulation, RSNA was inhibited to a greater extent and recovered more slowly than either hindlimb or thoracic SNA. These results suggest that RSNA resets less than BP, hindlimb, and thoracic SNA.
Although these studies suggest that BP may not acutely reset to the same extent as efferent SNA and that SNA to different regions may not acutely reset to the same degree, it is difficult to compare the extent of resetting of afferent baroreceptor activity, efferent SNA, and BP when these data are derived from different models and methodologies. Therefore, the purpose of this study was to evaluate acute resetting of the carotid baroreflex control of BP, ASNA, and RSNA in the same experimental model (unilateral isolated carotid sinus) and with the same methodology that has been previously used to characterize acute resetting in single-fiber carotid baroreceptor activity.
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Methods |
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General Methods
The effects of carotid baroreflex resetting were studied with a previously described unilateral vascularly isolated carotid sinus preparation17 in anesthetized mongrel dogs (25 mg/kg thiopental bolus plus 10 mg/kg per minute infusion). After anesthesia, the dogs were intubated and placed on a ventilator. The right femoral artery and vein were cannulated to permit measurement of arterial BP and infusion of anesthetic, respectively. Arterial blood gases were routinely monitored and maintained at physiological levels by adjustment of ventilation and infusion of sodium bicarbonate.
To isolate the carotid sinus region, we ligated the internal carotid, occipital, lingual, and facial arteries and other small branches emerging from the sinus region. Inflow and outflow cannulas were placed in the common carotid and external carotid, respectively, to permit a flow-through pulsatile perfusion of the carotid sinus region with the use of a servo-controlled roller pump (Sarns Instruments). A cannula inserted into the lingual artery allowed measurement of carotid sinus pressure. The isolated region was perfused with buffered lactated Ringer's solution oxygenated with 100% O2 to prevent activation of chemoreceptors that may not have been physically eliminated by the isolation procedure.18 Arterial and carotid sinus pressures were measured via the catheters inserted into the femoral and lingual arteries, respectively, and connected to Statham pressure transducers (Gould Instruments) and a polygraph (model 7D, Grass Instruments). So that baroreceptor input was limited to only the isolated sinus, the contralateral sinus was denervated and the vagosympathetic trunks were sectioned bilaterally. Sectioning of the vagosympathetic trunk eliminated the aortic baroreceptor input and also eliminated the possible effects of changes in efferent SNA on baroreceptor discharge.19
Efferent SNA was obtained by recording from the central end of the left ventral ansa subclavia or a branch of the left renal nerve. The ansa was approached via a thoracotomy consisting of removal of the first three or four left ribs. The ventral ansa was dissected from surrounding tissue, cut distal to the stellate ganglion at the midcervical ganglion so that the nerve would not contact adjacent tissue, immersed in oil in a bath constructed from surrounding tissue, and placed on tungsten-carbide recording electrodes. Although not used in any of the experiments, the dorsal ansa was also dissected from surrounding tissue and cut at the midcervical ganglion for possible use as an alternative to the ventral ansa. For recording of RSNA, a branch of the renal nerve was accessed by entering the peritoneal cavity abdominally. The intestines were retracted, and a nerve adjacent to the renal artery was dissected from surrounding tissue, cut proximal to the kidney, immersed in oil, and placed on tungsten-carbide recording electrodes.
The recording electrodes were connected via a high-impedance differential preamplifier (gain, 1000; 0.1- to 10-kHz pass band) and filter/amplifier (fourth-order Butterworth; 10-Hz to 3-kHz pass band) to an FM tape recorder (AR Vetter Co). Raw SNA, carotid sinus pressure, and BP were tape recorded for later computer analysis with a Hewlett-Packard 310 computer equipped with a 16-channel Infotek 12-bit A/D converter. SNA was analyzed by processing full wave–rectified nerve activity through a voltage-to-frequency converter with a gain of 10 kHz/V (maximum nonlinearity, 0.01%). The output frequency of the voltage-to-frequency converter (proportional to the total neural voltage) was sampled at 10 Hz by an 8-bit digital counter with D/A output and is presented as arbitrary units.
Data for stimulus-response curves were collected by recording baroreflex-induced changes in SNA and BP produced by a slow ramp increase in sinus pressure from 0 to 350 mm Hg. The slow ramp increase in sinus pressure (5 to 6 mm Hg/min) was generated by stopping the roller pump, allowing the carotid sinus pressure to fall to zero, clamping the outflow perfusion line, and using a syringe pump in-line (Harvard Instruments) with the inflow cannula to slowly infuse perfusate. Once sinus pressure reached 250 to 300 mm Hg, the syringe pump was turned off, the outflow line opened, and the roller pump turned on, returning to a constant mean pressure pulsatile perfusion.
Experimental Protocol
After the isolation procedure, the
carotid sinus was perfused
with a pulsatile pressure with a mean pressure equivalent to the
predenervation mean BP for a minimum of 30 minutes. For all dogs, this
was a mean sinus pressure between 100 and 125 mm Hg and considered to
be a mid CP. After this period, a pressure ramp was performed.
Pulsatile perfusion of the sinus region was then reestablished at a
sinus pressure that was randomly chosen at 50 mm Hg above (high CP) or
below (low CP) the initial sinus pressure by adjustment of outflow
resistance. The sinus region was reconditioned at the new CP for 20
minutes, followed by another pressure ramp. This process was repeated
for the remaining CPs. A 20-minute conditioning period was selected
because this was the conditioning period used for evaluation of
resetting in single-fiber carotid baroreceptors. Hence, the SNA and
BP responses to a slow ramp increase in sinus pressure were
recorded for at least three CPs: low (50 to 75 mm Hg), mid (100 to
125 mm Hg), and high (150 to 175 mm Hg). One half the dogs were
exposed to a sequence of CP changes from mid CP to high CP to low CP,
and the other half were exposed to a sequence of mid CP to low CP to
high CP. When possible, the dogs were exposed to a mid CP as the fourth
and final CP in the sequence.
Data Analysis
Stimulus-response curves were generated by
plotting sinus
pressure versus BP or SNA and using a sigmoidal curve-fitting
program18 for calculation of slope,
Pth, Psat,
P0.5, threshold BP or SNA, and saturation BP or SNA.
Additionally, the operating range of the reflex was determined by the
formula Operating Range=(Psat-Pth)/2. The
operating range is the range of sinus pressure over which reflex
changes in BP or SNA occur.
The curve fit parameters threshold BP (or SNA), saturation BP (or SNA), P0.5, and k [k=(4xSlope)/(Saturation BP-Threshold BP)] were averaged and used to generate the average stimulus-response curve for the corresponding CP and BP or SNA. Repeated measures ANOVA was used to identify differences in sigmoidal curve fit parameters among CPs for BP, RSNA, and ASNA. All statistical analyses were performed on a Macintosh IIci computer with SuperAnova software (Abacus Concepts).
Significant
changes in Pth were used as an index of
resetting. The extent of resetting was calculated as Fraction of
Resetting=Pth/CP. For example, when CP was
raised from the mid to high level, the fraction of resetting was
calculated as follows: Fraction of Resetting=[(CPhigh
Pth-CPmid
Pth)/(CPhigh-CPmid)]. Each
dog was exposed to two or three step changes in CP, and we used all
responses to determine average resetting values for both SNA and BP.
All data are presented as mean±SEM.
During our investigation, we noted that in dogs in which the ventral ansa had been cut for recording of ASNA, BP resetting was either attenuated or abolished. On analysis, we found that average BP resetting in ansa-sectioned dogs was significantly less. For that reason, we separated the BP data into two groups: BP from dogs in which the ASNA recordings were obtained (BPansa) and BP from dogs in which RSNA was obtained (BPrenal). To compare the extent of resetting of BP with that of SNA, we compared the fraction of resetting of BPrenal with the fraction of resetting of RSNA as well as the fraction of resetting of BPansa with the fraction of resetting of ASNA using ANOVA. Both renal and ansa nerve recordings were obtained in one dog. BP and ASNA data were included in the analysis; RSNA data were not included.
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Results |
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TopAbstractIntroductionMethods Results Discussion References |
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Average Stimulus-Response Curves
The average stimulus-response curves for the BPrenal, BPansa, ASNA, and RSNA responses to slow ramp increases in sinus pressure at varying CPs are shown in Figs 1
and 2. Note for all
variables (BP, ASNA, and RSNA) that as the CP increases, the
response curves shift to the right, in the direction of the CP change.
Select sigmoidal curve fit parameters, including
Pth and P0.5, which are used as indexes
of resetting, are presented in the Table.
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The average
stimulus-response curves for BPrenal are
presented in Fig 1A
. Pth and P0.5
increased as CP varied from low (Pth=105.1±9.2 mm Hg,
P0.5=162.4±10.3 mm Hg), to mid
(Pth=120.4±6.7,
P0.5=176.4±10.7), to high
(Pth=137.4±4.7,
P0.5=200.3±9.8). The low and
high Pth and P0.5 values were significantly
different (P<.05) from the mid Pth and
P0.5 values and from each other. The high-CP
Psat value was different from the mid- and low-CP
Psat values. The slope of the reflex response at high but
not low CP was significantly less than the slope at mid CP. The high-CP
saturation BP (100.4±4.6 mm Hg) was greater than the low-CP
saturation BP (90.9±5.1). Threshold BP and sinus pressure operating
range (Poper) did not differ among the three CPs.
The
stimulus-response curves for BPansa are
presented in Fig 1B, and the corresponding Pth and
P0.5 values are presented in the Table.
Pth and P0.5 increased as CP increased from low
(Pth=105.1±5.9 mm Hg,
P0.5=153.0±6.5
mm Hg) to mid (Pth=116.0±5.7,
P0.5=164.3±5.7). Pth and P0.5
at
high CP (Pth=120.7±5.2,
P0.5=171.0±10.5) did
not increase above mid-CP values but were significantly different from
low-CP values. The high-CP saturation BP (103.3±6.7 mm Hg) was
greater than the low-CP (83.9±6.3) and mid-CP (90.0±7.7)
saturation
BPs. Psat, slope, Poper, and
threshold BP did not differ among the three CPs. BPrenal
and BPansa did not differ for any of the curve fit
parameters listed in the Table.
The stimulus-response
curves for ASNA are presented in Fig 2A. Pth for the
mid-CP reflex (79.5±5.4 mm Hg) was
significantly different from that obtained for the low CP (71.2±6.2)
but not for the high CP (85.2±5.1) (Table), and
Pth values
for the high and low CPs were significantly different from each other.
This was also the case for P0.5 (Table). Although
the
slope tended to increase as CP increased, it was not
statistically significant. The low-CP threshold SNA was less than the
mid- and high-CP threshold SNAs. There were no significant differences
among any other parameter for the different CPs
(Table).
The stimulus-response curves for RSNA are shown
in Fig 2B, and the
corresponding Pth and P0.5 values are
presented in the Table. The reflex Pth values at
low (56.4±3.8 mm Hg) and high (100.6±7.7) CPs were significantly
different from each other and from the mid-CP value (77.0±4.1).
P0.5 at mid CP (116.2±4.9 mm Hg) was different from that
obtained at high CP (135.3±7.8) but not from that at low CP
(109.1±10.1). No significant changes were found for
Psat, Poper, slope, saturation
SNA, and threshold SNA with increasing CP for RSNA (Table).
RSNA and ASNA did not differ significantly for any curve fit
parameter listed in the Table.
Fraction of Resetting
Section of the left ventral ansa
significantly attenuated the
average fraction of resetting for BP (Fig 3;
BPansa, -0.202±0.034 versus
BPrenal, -0.335±0.046). This was primarily
attributed to a loss of upward resetting in response to increases in CP
(Fig 4). When the ansa was sectioned, the fraction of
resetting for decreases in CP was 0.281±0.042, and the fraction of
resetting for increases in CP was 0.106±0.034, significantly less than
the fraction of resetting for increases in CP when the ansa was intact.
Thus, sectioning of the ansa significantly reduced the fraction of
resetting in response to increases in CP; therefore, we separated the
BP data into two groups to analyze the fraction of resetting.
The sequence of CPs did not significantly affect the fraction of acute
resetting of BP or SNA.
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) vs
denervated (BPansa, 
). BP reset to a
greater degree when the ansa was intact (n=18, 0.335±0.046)
compared
with when denervated (n=20, 0.194±0.031). Data are
mean±SEM,
P<.05. *Significantly different from left ansa
intact.
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Fig 5 presents the average
fractions of resetting
for BPrenal (n=18, 0.335±0.046), RSNA (n=20,
0.506±0.072), BPansa (n=22, 0.194±0.031), and
ASNA
(n=21, 0.200±0.057) that occurred for all changes in CP. There
were no differences in resetting for increases or decreases in CP for
ASNA (increases=0.164±0.051,
decreases=0.232±0.100) or RSNA
(increases=0.534±0.120, decreases=0.478±0.087).
For experiments in
which only renal nerve recordings were obtained, RSNA resetting
was significantly greater than BPrenal resetting. For
experiments in which ansa nerve recordings were obtained, ASNA
was not different from BPansa. In one dog, both renal and
ansa nerve recordings were obtained at three different CPs,
giving two fraction of resetting values. In this dog, the average
fraction of resetting values were as follows: BP=0.114±0.016,
RSNA=0.210±0.002, and ASNA=0.134±0.003. These
values are within 1 SD
of the values reported in this investigation and follow the same
pattern: BP and ASNA reset to a similar extent but less than RSNA.
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Discussion |
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This study has found that there is differential resetting of BP, ASNA, and RSNA, with RSNA resetting to a greater extent than either BP or ASNA. Using a unilateral isolated sinus preparation with a pulsatile perfusion pressure, we found values for average resetting of BP (0.20 to 0.34) that are comparable to values others have found using similar preparations. Tan et al14 reported an average resetting of 0.25 measuring changes in set point pressure, Pth, and range midpoint BP (BP0.5) in anesthetized dogs with a bilaterally isolated carotid sinus and static perfusion pressure. Using the bilaterally isolated carotid sinus preparation with a static perfusion pressure in normotensive anesthetized dogs, Brunner and Kligman6 found that BP reset between 0.16 and 0.22. As with other studies,6 13 14 we also noticed a tendency for a greater shift in Pth at the low compared with the high CP; however, this trend was not significant.
Resetting of efferent SNA has been reported in various species. With a few exceptions,4 5 8 15 previous investigations regarding resetting of SNA have not evaluated the extent of resetting as shifts in the dynamic response curves (eg, shifts in Pth, P0.5, etc, of the stimulus-response curves) but rather as a degree of suppression of baseline nerve activity after a baroreceptor stimulus.7 20 When the dynamic response was evaluated, a quantitative index of resetting (ie, fraction of resetting) was not always reported. The degree of SNA suppression after an increase in carotid sinus pressure is inversely proportional to the extent of resetting. If little resetting occurs, then nerve activity will remain suppressed after an increase in CP. However, if resetting is complete (1.00), then nerve activity will return to previous levels despite the increased CP. Kunze7 reported a prolonged suppression of RSNA compared with BP after aortic nerve stimulation, which suggests that RSNA resets less than BP. Conversely, in the present study we found that RSNA resetting (0.50) is significantly greater than BP resetting (0.20 to 0.34). We also found that ASNA resets at 0.20, significantly less than RSNA but not different from BP. An important question to be addressed in future studies is the relationship of change in nerve activity to change in local resistance and hence control of pressure.
Effect on Reflex Sensitivity
Evidence is equivocal regarding
the effect of acute resetting on
baroreflex changes in sensitivity for
BP6 13 21 and
efferent SNA.4 15 20 Although we found
that the slope of
the stimulus-response curve for BPrenal at high CP was
attenuated, we did not observe any effect of changes in CP on reflex
sensitivity of RSNA or ASNA.
Role of Pulsatile Perfusion Pressure
Reports comparing the
effect of pulsatile versus static perfusion
pressure on baroreceptor resetting indicate that there is either no
difference1 22 or pulsatile pressure attenuates
baroreceptor resetting.23 Mendelowitz and
Scher9 reported that a pulsatile perfusion pressure
prevents carotid baroreflex resetting 5 minutes after a change in CP
when a unilateral isolated sinus preparation is used in the rabbit.
However, other investigators have also reported that baroreflex
resetting occurs 15 to 20 minutes after a change in CP with the use of
pulsatile pressures in an isolated sinus
preparation.8 13
In the current study, we observed significant reflex resetting 20
minutes after a change in CP. It is possible that the pulsatile
pressure prevents rapid resetting, ie, within 5 minutes, and although
it may attenuate acute resetting, it does not prevent acute resetting
over longer conditioning periods.
An important observation from our study is the effect on BP resetting of sectioning the left ansa subclavia. The ansa subclavia contains both efferent and afferent sympathetic fibers innervating a wide variety of thoracic structures, including both heart chambers, coronary and pulmonary vessels, and the great vessels.24 25 26 When the ansa was intact, average BP resetting (0.335) was significantly greater than when the ansa was sectioned (0.194). Moreover, there was a directional sensitivity with ansa denervation. Although downward resetting (0.281±0.042) was relatively unaffected, upward resetting (0.106±0.034) of BP was significantly attenuated compared with upward resetting when the ansa was intact. Since efferent sympathetic drive from the left ansa subclavia contributes to changes in heart rate, myocardial contractility, and vascular resistance, which mediate baroreflex-induced changes in BP, differences in the fraction of resetting of BP might be explained by loss of thoracic efferent SNA. However, there was no loss of dynamic control, ie, the ability to reflexly alter BP during the sinus pressure ramp, as evidenced by no significant change in the slope or maximum (threshold BP) (P=.64) and minimum (saturation BP) (P=.83) arterial pressures at the different CPs generated during the ramp, suggesting that loss of efferent activity is probably not mediating the reduced BP resetting.
Sectioning the ansa eliminates cardiopulmonary sympathetic afferent activity as well as efferent activity. At this time, relatively little is known regarding the central pathways or physiological role of cardiac sympathetic afferents. However, it is known that cardiopulmonary receptors with sympathetic afferents are widely distributed in the atria, ventricles, coronary and pulmonary vessels, and great vessels.25 These receptors are chemosensitive mechanoreceptors that mediate cardiac pain produced by myocardial ischemia,27 produce hypertension and tachycardia,27 28 increase RSNA29 upon stimulation, and attenuate baroreflex control of heart rate.30 Blockade of all cardiac receptors with either vagal or sympathetic afferents results in enhanced baroreflex control of RSNA.15 31 32 However, the contribution of receptors with sympathetic afferents in the modulation of baroreflex control of RSNA is unknown. We did not determine the effect of sectioning the ansa on RSNA resetting in this study because ASNA and RSNA were recorded in separate dogs. We speculate that a loss of sympathetic afferent input to the central nervous system may remove a tonic inhibition on baroreflex control of BP, which resulted in enhanced dynamic baroreflex control of BP. This is suggested by a trend (P=.20) for a greater slope and more narrow Poper (P=.06) for the sinus pressure–BPansa relationship compared with the sinus pressure–BPrenal relationship.
Using the same experimental model that has been used previously to measure acute resetting in types 1 and 2 carotid baroreceptors, we evaluated acute resetting of carotid baroreflex control of BP, RSNA, and ASNA. A previous investigation from our laboratory demonstrated that type 1 carotid baroreceptors acutely reset at 0.12 to 0.15.1 In the present investigation, we demonstrate that BP resets at 0.20 to 0.34, RSNA 0.50, and ASNA 0.20. The differences in the fraction of resetting between the afferent and efferent limbs of the baroreflex may be accounted for by central facilitation. Most investigations suggesting the involvement of a central component in acute resetting are based on prolonged suppression of efferent SNA or BP after baroreceptor stimulation7 or at the end of the stimulation interval.5 33 However, a few investigations have directly established a central component.8 34 The central component of baroreflex resetting refers to a central nervous system–mediated facilitation of baroreceptor activity. Tan et al8 performed a study in conscious dogs in which the CP was held constant in the right carotid sinus and the left carotid sinus was conditioned at different pressures for 20 minutes. When a pressure ramp was performed on the right sinus (the nonresetting sinus), the Pth for the sinus pressure–mean BP response curve reset 0.46 to 0.61 because of the sustained changes in left sinus pressure. Hayward et al34 evaluated carotid baroreflex–induced changes in BP and RSNA after aortic nerve stimulation and found that the sinus pressure–BP stimulus-response curve shifted upward and rightward, with a significant increase in P0.5. The sinus pressure–RSNA stimulus-response curve shifted downward, with no change in Pth or P0.5. These two studies indicate that central neurons involved in mediating the baroreflex can be reset by signals arising from another baroreceptor group and further suggest that resetting of baroreceptor activity alone does not account for reflex resetting. Using preparations with only one functioning group of baroreceptors, Heesch and Barron5 and Kunze7 also demonstrated a central facilitation of baroreceptor activity, suggesting that central neurons mediating the baroreflex can be reset by signals arising from the same group of baroreceptors. Therefore, centrally mediated facilitation of baroreceptor activity might account for the greater extent of acute resetting of BP, ASNA, and RSNA compared with acute resetting of baroreceptor activity. Alternatively, the disparity between the extent of acute resetting of baroreceptor activity and efferent SNA and BP may reflect the lack of a one-to-one relationship of baroreceptor input to output, either at the level of the first termination of baroreceptor afferents on nucleus tractus solitarius neurons or at other distal steps in the signaling process. Very little is known about the central processing of baroreceptive information, ie, the extent of convergence and divergence of afferent activity or the temporal and spatial interactions of functionally or anatomically different baroreceptors and different barosensitive receptor groups (carotid, aortic, cardiac).
The finding that ASNA does not reset to the same extent as RSNA suggests that there may be differential carotid baroreflex control of SNA. Previous investigations have identified a viscerotopic organization of sympathetic motoneuron pools in the ventrolateral medulla.35 36 37 The differential carotid baroreflex control of regional SNA may be due to a disproportionate projection of baroreceptor input to organ-specific sympathetic motoneuron pools. Furthermore, the fact that acute baroreceptor resetting occurs in the type 1 but not type 2 baroreceptor suggests that the type 1 receptor mediates the differential control. Differential control, which implies a nonuniform autonomic response to activation of barosensitive receptors, has been demonstrated in the control of SNA,7 38 39 40 vascular resistance, and blood flow41 42 43 to the renal, splenic, hindlimb, and cardiac beds.
In summary, we found differential control of carotid baroreflex resetting of ASNA and RSNA with acute changes in sinus pressure in the thiopental-anesthetized dog using a unilateral vascular isolated carotid sinus preparation. The manner in which this differential control of SNA contributes to the acute resetting of BP must be determined. However, the finding that ASNA and RSNA are regulated differently during resetting suggests that there may be differential regulation of these outflows during other conditions, leading to functionally specific changes in SNA.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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This work was supported by VA Medical Research funds and a Predoctoral fellowship from the American Heart Association, Wisconsin Affiliate. We thank Claudia A. Hermes for technical assistance.
Received July 6, 1995; first decision August 15, 1995; accepted October 31, 1995.
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References |
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TopAbstractIntroductionMethods Results Discussion References |
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