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Department of Physiology, Graduate School of Health Sciences, Hiroshima University, Hiroshima 734-8551, Japan
Submitted 23 March 2004 ; accepted in final form 26 May 2004
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ABSTRACT |
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-adrenergic blockade but abolished by muscarinic blockade, suggesting that the bradycardia is mainly evoked through cardiac vagal outflow. We conclude that central command, produced within the caudal diencephalon and the brain stem, selectively inhibits the cardiac component, but not the vasomotor component, of the aortic baroreflex at the onset of spontaneous exercise. baroreflex bradycardia; baroreflex depressor response; central command; exercise pressor reflex; decerebrate cats
It has been reported that the exercise pressor reflex or central command modulates the arterial baroreflex, which is characterized by a threshold pressure, operating point, and gain (24, 25, 27, 29). The stimulus-response curve of the carotid sinus baroreflex was reset, but the gain was unaffected, by ischemic dynamic or static exercise in human subjects (4). A resetting of the carotid baroreflex curve during dynamic and static exercise was also observed in another study, and the magnitude of this resetting was reduced by epidural anesthesia (31). Previous studies using anesthetized rats (21) and decerebrate cats (17) have shown that the gain of the arterial baroreceptors-HR reflex was reduced during electrically evoked muscle contraction or during stimulation of the peroneal nerve. Considered together, these studies suggest that the exercise pressor reflex resets the stimulus-response curve of the arterial baroreflex and blunts the baroreflex gain. On the other hand, central command may also reset the carotid baroreflex during static and dynamic exercise as demonstrated by studies using human subjects who had received partial neuromuscular blockade (5, 28) or by patellar tendon vibration (23). However, the aforementioned studies addressed baroreflex modulation during the steady-state period of exercise, which may be different from the effects at the beginning of exercise.
The decerebrate cat model, in which the cerebrum and the rostral part of the diencephalon are interrupted from the brain stem, can generate spontaneous overground locomotion that is accompanied by increases in HR and AP (15, 30). These immediate increases in cardiovascular function are thought to be mediated by central command (15, 30), thus making this a good model to examine the influence of central command on arterial baroreflex function. Our laboratory demonstrated that the centrally induced increase in HR elicited by spontaneous locomotion was attenuated by sinoaortic denervation, whereas the pressor response was exaggerated, suggesting that central command modulates baroreflex function (15, 30). Recently, our laboratory reported that the baroreflex bradycardia due to stimulation of the aortic depressor nerve (ADN) is blunted immediately before or at the onset of voluntary static exercise using conscious cats (11). Similarly, the response of the R-R interval to a step increase in carotid sinus transmural pressure is transiently reduced at the beginning of isometric handgrip exercise in humans, even in the anticipation period preceding the start of exercise (3, 13). Thus the attenuating effect on the baroreflex bradycardia seen immediately before the onset of exercise strongly leads to a hypothesis that the gain of the arterial baroreceptors-HR reflex is temporarily decreased by central command, which in turn contributes to an increase in HR.
It is difficult to precisely discriminate the influence of central command on arterial baroreflex function from that of the exercise pressor reflex because mechanosensitive muscle afferent neurons are activated once muscular contraction begins. To address this, we analyzed arterial baroreflex function using unanesthetized, decerebrate (precollicular-premammillary) cats. These animals can spontaneously contract skeletal muscle, and the initial cardiovascular responses are primarily mediated by central command. Aortic baroreflex function was assessed by determining the bradycardia and depressor response elicited by electrical stimulation of the ADN, and alterations in baroreflex function at the onset of spontaneous muscle contraction were interpreted as being mediated by central command. To activate the exercise pressor reflex and thus examine its effect on the baroreflex, we passively stretched the triceps surae muscle or electrically induced a contraction of this muscle. Muscle stretch primarily activates muscle mechanoreceptors, whereas muscle contraction activates both muscle mechanoreceptors and metaboreceptors (10).
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METHODS |
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Preparations
For the implantation of catheters, the decerebration, and preparation of the left aortic nerve, the cats were anesthetized by inhaling a halothane (4%)-N2O (1 l/min)-O2 (1 l/min) gas mixture. An endotracheal tube was inserted into the airway, and an electrocardiogram, HR, and respiration were continuously monitored. To ensure a surgical level of anesthesia, halothane was increased in a range of 1.0–2.5% if HR and/or respiration spontaneously increased and/or if limb withdrawal occurred in response to a noxious pinch of the paw. Polyvinyl catheters were inserted into the right femoral vein for administering drugs and into the right femoral artery for measuring arterial blood pressure (AP). The right femoral artery catheter was connected to a pressure transducer (model DPT III, Baxter, Tokyo, Japan). HR was derived from the AP pulse with a tachometer (model 1321, GE Marquette Medical Systems, Tokyo, Japan). Rectal temperature was maintained at 37–38°C with a heating pad and a lamp. The head of the cat was then mounted on a stereotactic frame. As described in detail previously (15, 20, 30), decerebration was performed by electrocoagulation at the precolliculr-premammillary body using the following stereotaxic coordinates (1): 13 mm anterior, 6 mm horizontal, and 1–11 mm lateral, with a 14° angle from the perpendicular line. At the end of each experiment, the animal was killed with an overdose of pentobarbital sodium and the transected area of the brain was examined histologically. We confirmed that the cerebral cortex, the rostral parts of the thalamus, and the hypothalamus (the anterior hypothalamic area, the supraoptic nucleus, and the rostral part of the lateral hypothalamic area) were disconnected from the brain stem as previously reported (20).
After the decerebration was completed, the cat was removed from the stereotactic frame and placed in the lateral posture. The left ADN was dissected from surrounding connective structures at the cervical level. A pair of Teflon-coated silver-wire electrodes was implanted on the ADN bundle for electrical stimulation. After confirmation of the characteristic discharge of the ADN, the nerve bundle was cut at the peripheral side of the electrodes, and the nerve-electrode complex was covered with silicone gel. The tibial nerve innervating the left triceps surae muscle was dissected from the sciatic nerve at the popliteal fossa. A pair of Teflon-coated silver-wire electrodes was implanted on the tibial nerve bundle to electrically evoke a contraction of the left triceps surae muscle. The calcaneus tendon and bone were exposed and isolated from surrounding tissue. The tension of the triceps surae muscle was measured by a force transducer (model LC1205-KC50, A&D, Tokyo, Japan) attached to the cut calcaneus bone. In addition, a pair of Teflon-coated silver wire electrodes was inserted into the triceps surae muscle for recording electromyogram (EMG). The original EMG was amplified by a differential preamplifier (model S-0476, Nihon Kohden, Tokyo, Japan) with a band-pass filter of 50–3,000 Hz. The amplified output was rectified and integrated with a resistance-capacitance integrator having a time constant of 20 ms. Inhalation anesthesia was stopped once the surgical procedures were completed. The experiments were started 5–7 h after the cessation of halothane anesthesia.
Aortic baroreceptor afferent neurons were electrically stimulated by using a train of electrical pulses at a frequency of 50 Hz for 1 s (5 ± 1 V; 0.2-ms duration). HR decreased in response to this stimulation with a 2–5 beat latency, whereas the latency for the depressor response was 3–10 beats. The magnitude of the baroreflex bradycardia and depressor response during rest, i.e., no other perturbation to the animal, was defined as the control response. ADN stimulation was then repeated during bouts of spontaneous contraction, electrically evoked contraction, or passive muscle stretch to determine the effect on arterial baroreflex function. Multiple trials were performed on each animal.
HR, AP, EMG, muscle tension and a marking signal for the onset and offset of the ADN stimulation were continuously recorded on an eight-channel pen-writing recorder (model Recti-8K, GE Marquette Medical Systems, Tokyo, Japan). The data were also stored in a computer with an analog-to-digital converter (model MP100, BIOPAC Systems, Santa Barbara, CA) at a sampling frequency of 1 kHz. The beat-to-beat calculated parameters of HR, systolic AP (SAP), mean AP (MAP), and diastolic AP (DAP) were stored on a hard disk by using a software program (AcqKnowledge 3.7.0, BIOPAC Systems) for offline analysis.
Protocols
The cat was placed in the lateral posture. The pelvis, knee, and ankle joints were clamped to prevent body trunk and hindlimb movement during muscle contraction or passive stretch of the triceps surae muscle. The initial tension loaded to the triceps surae muscle was set at 1 kg.
Spontaneous static contraction. The decerebrate cats were able to evoke spontaneous muscle contraction without any kind of artificial stimulation. To evaluate the effect of spontaneous static contraction on the central properties of the aortic baroreflex, ADN stimulation was given before, at the onset of, and after spontaneous static contraction (n = 33 trials in 8 cats). The average duration of spontaneous static contraction was 5.8 ± 0.6 s. In each trial, the ADN stimulation was delivered automatically or manually as soon as the EMG activity of the triceps surae muscle increased.
Electrically evoked static contraction and passive stretch. To identify the effect of the exercise pressor reflex on aortic baroreflex function, ADN stimulation was induced during electrically evoked static contraction (n = 17 trials in 6 cats) or passive stretch (n = 12 trials in 5 cats). Static muscle contraction was induced by stimulating the left tibial nerve for 30 s (intensity, 1.5x motor threshold; duration, 0.2 ms; frequency, 20–40 Hz). ADN was stimulated at the onset of the electrically evoked muscle contraction with the same procedure as spontaneous muscle contraction. Moreover, ADN stimulation was repeated 15 s after the onset of the evoked contraction. In the case of passive stretch, the triceps surae muscle was mechanically stretched 1 cm for 30 s by using a manipulator. The ADN stimulation was induced at the onset of passive stretch and 15 s from the first stimulation.
The same protocols were repeated after injections of propranolol hydrochloride (0.5–1.0 mg/kg iv) and atropine sulfate (0.1 mg/kg iv) to examine a relative contribution of cardiac sympathetic and parasympathetic outflows to the ADN-induced baroreflex bradycardia at the onset of spontaneous static contraction in four cats.
Data Treatment and Statistical Analysis
HR, AP, muscle tension, and the marking signal for ADN stimulation were displayed on a computer screen. The start and end of muscle contraction or passive stretch were visually determined using the signals of EMG activity and/or muscle tension. The average values of HR and SAP obtained for 30 beats before the onset of static contraction or passive stretch were defined as the baseline levels. These data were classified into the three groups (spontaneous contraction, electrically evoked contraction, and passive stretch). In each group, the beat-to-beat changes in HR and SAP from the baseline levels in a given trial were aligned at the onset of ADN stimulation and then averaged. Their beat-to-beat responses to ADN stimulation were compared between resting and a muscle intervention using a two-way ANOVA. The peak change in HR in response to ADN stimulation given during the muscle intervention was defined as 
HRpeak. The time at which HRpeak was detected was defined as Tpeak. The mean change in HR at Tpeak during the identical muscle intervention without ADN stimulation was defined as HRref. Therefore, the net decrease in HR (HRnet) due to ADN stimulation during the muscle intervention was calculated as (HRnet = HRref – HRpeak). The net decrease in SAP (SAPnet) was also calculated in the same manner [SAPnet = SAPref – SAPpeak]. The peak values of HRnet and SAPnet for each muscle intervention were expressed as relative percent values against the 100% control responses to the ADN stimulation observed during resting. The relative percent values were compared by a one-way ANOVA among resting and the three muscle interventions. When a significant F value in the main effect of muscle intervention was present, a Tukey's post hoc test was performed to detect a significant difference in the relative peak values from the control. The level of statistical significance was defined as P < 0.05. The data are expressed as means ± SE.
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RESULTS |
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The baseline and peak values of HR, SAP, MAP, and DAP during spontaneous or electrically evoked muscle contraction or passive stretch are summarized in Table 1. HR and MAP increased during spontaneous static contraction by 22 ± 3 beats/min and 32 ± 3 mmHg from the baseline values, respectively. Similar to spontaneous contraction, HR increased by 22 ± 3 beats/min during the electrically evoked contraction and by 24 ± 6 beats/min during passive stretch. Likewise, MAP rose by 33 ± 3 and 22 ± 6 mmHg during the electrically evoked contraction and passive stretch, respectively. The tachycardia and depressor response were not different among the three muscle interventions, although the pressor response during passive stretch tended to be smaller than the others. Muscle tension developed during the electrically evoked contraction or passive stretch was much greater than during spontaneous contraction.
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ADN stimulation at rest decreased HR and AP. In Fig. 1, A and B, the first two traces show an example of the reductions in HR and AP in response to ADN stimulation preceding muscle activity. The ADN stimulation-induced bradycardia and depressor response were 40 ± 2 beats/min and 11 ± 1 mmHg (n = 62 trials in 8 cats), respectively. The latency for the bradycardia was 3.1 ± 0.2 beats from the onset of ADN stimulation, whereas that of the depressor response was 6.5 ± 0.7 beats.
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As demonstrated in Fig. 1A, the ADN stimulation-induced baroreflex bradycardia was attenuated at the onset of spontaneous muscle contraction. After the cessation of the muscle contraction, the bradycardia response to ADN stimulation was restored. Figure 2A compares the time courses and amplitudes of the beat-to-beat changes in HR to ADN stimulation during resting and spontaneous contraction. The HR response during spontaneous contraction without the ADN stimulation is superimposed on the same panel. The peak decrease in HR (HRpeak) in response to ADN stimulation given at the onset of spontaneous contraction was 10 ± 3 beats/min. Because HR at the onset of spontaneous contraction without the ADN stimulation was increased by 7 ± 2 beats/min (HRref), the ADN stimulation-induced net bradycardia (HRnet) at the onset of spontaneous contraction was 17 ± 3 beats/min, which was much smaller (P < 0.01) than the bradycardia of 36 ± 3 beats/min observed during rest. In contrast, the ADN stimulation-induced depressor response was not affected by spontaneous static contraction (Fig. 1A). The increase in SAP during spontaneous contraction without ADN stimulation (SAPref) was 21 ± 4 mmHg, whereas the increase in SAP was reduced to 11 ± 3 mmHg (SAPpeak) by ADN stimulation evoked at the onset of spontaneous contraction (Fig. 3A). The net amplitude of the ADN stimulation-induced depressor response (SAPnet) was 10 ± 3 mmHg, which was not significantly different (P = 0.53) compared with the control response of 7 ± 2 mmHg.
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Effects of Electrically Evoked Static Contraction and Passive Stretch on the ADN Stimulation-Induced Bradycardia and Depressor Response
The ADN stimulation-induced bradycardia and depressor responses during electrically evoked contraction were not different compared with rest (Fig. 1B). Figure 2B represents the time courses and amplitudes in the beat-to-beat changes of HR due to ADN stimulation given during rest and electrically evoked contraction. The HR response during electrically evoked contraction without ADN stimulation is superimposed. ADN stimulation given before muscle contraction produced a baroreflex bradycardia of 34 ± 6 beats/min. The ADN stimulation given at the onset of electrically evoked contraction decreased HR by 28 ± 5 beats/min (HRpeak), and there was no significant influence of electrically evoked contraction on the net amplitude of the ADN stimulation-induced bradycardia (HRnet, 30 ± 6 beats/min). The ADN stimulation-induced depressor response (SAPpeak) was 6 ± 2 mmHg at the onset of electrically evoked contraction (Fig. 3B). The net depressor response (SAPnet) produced by ADN stimulation was 11 ± 3 mmHg, which was not different (P = 0.18) from the control depressor response of 6 ± 3 mmHg. The baroreflex bradycardia and depressor response to ADN stimulation given at the onset of passive stretch had almost the same results as those during electrically evoked contraction. Figures 2C and 3C show the time courses and amplitudes of the beat-to-beat changes in HR and SAP to the ADN stimulation given at the onset of passive stretch. There were no significant differences in HRnet and SAPnet during rest and at the onset of passive stretch.
The ADN stimulation-induced bradycardia and depressor response at rest were defined as 100%, and the relative percent values among the three muscle interventions are summarized in Fig. 4. The ADN stimulation-induced baroreflex bradycardia was significantly inhibited at the onset of spontaneous static contraction to 55 ± 4%. However, this attenuating effect of the baroreflex bradycardia was not observed at the onset of either electrically evoked static contraction or passive stretch. Furthermore, when ADN stimulation was given at the middle of electrically evoked contraction or passive stretch, the attenuating effect on the baroreflex bradycardia was not induced. The ADN stimulation-induced baroreflex depressor response was not modified by any of the muscle interventions (spontaneous and electrically evoked contraction and passive stretch).
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DISCUSSION |
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-adrenergic blockade but was abolished by muscarinic blockade, indicating that the modulation of the aortic baroreceptors-HR reflex is predominantly evoked through cardiac parasympathetic nerve activity. The aortic baroreceptors-HR reflex is temporally inhibited immediately before or during the early period of voluntary exercise in humans and conscious cats (3, 11, 13). The baroreflex-induced rise in the R-R interval to a step increase in carotid sinus transmural pressure is blunted at the beginning of isometric handgrip exercise in humans, even in the anticipation period preceding the start of exercise (3, 13). Moreover, our recent study (11) demonstrated that the baroreflex bradycardia induced by ADN stimulation is temporarily attenuated to 62 ± 5% of control at the onset of voluntary static exercise in conscious and intact cats. We found that the most marked degree of baroreflex blunting occurs immediately before or at the onset of muscular activity associated with volitional exercise (11). Thus it is likely that inhibition of the arterial baroreceptors-HR reflex is mediated by central command at the onset of static exercise in conscious humans and cats. Although the cerebral cortex is believed to have an important role in controlling somatic movement during voluntary exercise, it was unclear whether the cerebrum was also essential for the attenuated baroreflex bradycardia at the beginning of exercise. To solve this question, we attempted to examine whether the same attenuated baroreflex bradycardia was observed at the onset of spontaneously evoked static contraction using decerebrate cats. Indeed, the ADN stimulation-induced baroreflex bradycardia was blunted to 55 ± 4% of the precontraction bradycardia at the onset of spontaneous static contraction in decerebrate cats, indicating that the attenuating effect of central command on the reflex bradycardia is observed in decerebrate, as well as conscious, intact cats (11). This result implies that some central site(s) in the caudal part of the diencephalon and the brain stem can generate a descending signal that modulates the cardiac component of the aortic baroreceptors-HR reflex. This is further supported by our laboratory's previous study using the decerebrate cat model, which showed that the increase in HR at the onset of overground locomotion was attenuated by sinoaortic denervation (15, 30). This effect of sinoaortic denervation on the HR response suggests that the arterial baroreceptors-HR reflex is inhibited by central command, which in turn contributes to the initial tachycardia at the onset of locomotion (15, 30).
The effect of central command on the stimulus-response curve of the carotid sinus baroreflex has been investigated during the steady-state period of exercise in humans and decerebrate cats (5, 16, 28). Augmented central command during exercise in humans with partial neuromuscular blockade caused a resetting of the stimulus-response curve of the carotid baroreflex to a higher blood pressure without changing the gain (5, 28). This type of resetting of the carotid baroreflex was similarly observed during electrical stimulation of the mesencephalic locomotor region in decerebrate cats (16). However, it remains unknown whether the blunted bradycardia to ADN stimulation at the onset of spontaneous contraction observed in decerebrate, as well as conscious, intact cats is caused either by a resetting of the stimulus-response curve of the arterial baroreflex toward a higher blood pressure or by a reduction in the slope of the baroreflex curve. If a resetting of the baroreflex curve may take place at the onset of spontaneous contraction, the reduction of the ADN stimulation-induced bradycardia would be explained by shifting the operating point beyond the quasilinear range of the reset baroreflex curve. Alternatively, a reduction in the slope is applicable irrespective of the blood pressure range, and AP is not raised yet at the onset of spontaneous contraction. To answer this issue, we recently conducted a preliminary study using conscious cats. We examined the dynamic characteristics of the stimulus-response curve of the arterial baroreflex at the onset of voluntary static exercise by lowering or elevating AP due to infusion of sodium nitroprusside or phenylephrine. As a matter of fact, we found that a threshold blood pressure of the baroreflex curve did not alter at the onset of exercise but the gain was reduced (unpublished observation). We consider, therefore, that the gain of the stimulus-response curve of the aortic baroreflex is temporarily suppressed at the onset of spontaneous exercise by central command.
The ADN stimulation-induced baroreflex bradycardia was blunted at the onset of spontaneous muscle contraction, whereas the depressor response induced by the ADN stimulation was not affected. Similarly, voluntary static exercise did not affect the baroreflex depressor response evoked by an increase in carotid sinus transmural pressure in humans (12, 33) or by ADN stimulation in conscious cats (11), although the baroreflex bradycardia was blunted at the onset of voluntary exercise. Our laboratory previously reported that sinoaortic denervetion blunts the centrally induced initial tachycardia at the beginning of spontaneous overground locomotion in decerebrate cats, although the response in AP is augmented (15, 30). These contrasting effects on the responses between HR and AP suggest that the two components (cardiac vs. vasomotor) of arterial baroreflex are differentially controlled during spontaneous exercise. Thus it is likely that central command selectively inhibits the cardiac component of the arterial baroreflex, but not the vasomotor component, at the onset of spontaneous exercise; accordingly, central command may affect the cardiac-specific baroreflex pathway in the brain stem rather than it may cause a generalized modulation over the whole pathways.
Once muscular exercise starts, the possibility that a reflex activation of muscle afferent fibers modifies the arterial baroreflex cannot be neglected. If input from muscle mechanoreceptors and/or metaboreceptors contributes to the modulation of the reflex bradycardia, the ADN stimulation-induced bradycardia would be altered during an electrically evoked contraction or passive stretch. The baroreflex bradycardia during electrically evoked contraction or passive stretch was not different from the control response in the present study. This suggests that the exercise pressor reflex arising from muscle mechanoreceptors and metaboreceptors has little or no influence on the gain of the arterial baroreceptors-HR reflex. Previous studies support this concept as they showed that the exercise pressor reflex resets baroreflex curve without altering baroreflex gain (4, 7, 16, 25, 29, 31). On the other hand, Nosaka and Murata (21) reported that the ADN stimulation-induced baroreflex bradycardia is reduced during electrically evoked muscle contraction in anesthetized rats, suggesting an attenuated baroreflex gain by muscle afferent input. The inhibition of the baroreflex bradycardia was observed 3–4.5 min after the onset of the evoked contraction. We did not observe any modulation of the ADN stimulation-induced bradycardia at the onset or 15 s after the onset of electrically evoked contraction. If the evoked contraction was prolonged over several minutes, then a reflex-induced reduction in gain may have been observed.
Regarding a central mechanism responsible for modulation of the arterial baroreflex function, it has been demonstrated that the baroreflex bradycardia elicited by electrical stimulation of the carotid sinus nerve or ADN or by elevation of carotid sinus pressure is inhibited by activation of some central sites, such as the hypothalamic defense area and the dorsolateral part of the midbrain periaqueductal gray matter (2, 6, 8, 22). Baroreceptor-sensitive neurons in the nucleus tractus solitarius receive an inhibitory action from the hypothalamus, which is mediated with a GABAergic mechanism (18, 32). In addition, the descending inputs to the nucleus tractus solitarius from the hypothalamus and midbrain do not involve GABA-containing fibers (9, 32). Thus an integrative circuitry within the nucleus tractus solitarius involving GABA-containing interneurons may play a role in central modification of arterial baroreflex function (26, 32). On the other hand, the vagal bradycardia evoked by microinjection of glutamate into the nucleus ambiguus was blunted by stimulation of the midbrain periaqueductal gray matter (8). This finding suggests that vagal cardiac preganglionic motoneurons in the nucleus ambiguus are a target for an inhibitory action from the midbrain periaqueductal gray matter. In the present study, the inhibition of the cardiac component of the aortic baroreflex at the onset of spontaneous contraction tended to be maintained after -adrenergic blockade and was abolished by muscarinic blockade, suggesting a dominant role of cardiac parasympathetic nerves in causing the baroreflex bradycardia due to ADN stimulation. We considered that central command descending from higher brain centers, which are supposed to be in the caudal part of the diencephalon and the brain stem, may inhibit an activity of the baroreceptor-sensitive neurons in the arterial baroreflex arc. However, whether this inhibitory influence is a direct action on cardiac parasympathetic preganglionic neurons in the nucleus ambiguus or whether it involves the nucleus tractus solitarius is not known at present.
In summary, the baroreflex bradycardia due to the aortic nerve stimulation was blunted at the onset of spontaneous muscle contraction, but not electrically evoked contraction or passive stretch, in decerebrate cats. We conclude that central command, generated at the onset of spontaneous exercise, plays an important role in the blunted sensitivity of the cardiac component of the aortic baroreflex, which in turn contributes to an increase in heart rate from the onset of exercise.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
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) and during muscular work (
). Furthermore, HR response during each muscle intervention without the ADN stimulation (
) is superimposed on the same panel. Arrows, ADN stimulation. Duration of spontaneous or electrically evoked muscle contraction or passive stretch is shown by the horizontal bar. A: amplitude of the ADN stimulation-induced baroreflex bradycardia was decreased at the onset of spontaneous contraction. B and C: attenuating effect of the baroreflex bradycardia was not observed at the onset of the electrically evoked contraction or passive stretch.
