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The effect of increasing the innervation field sizes of nerves on their reflex response time in salamanders.

1. A simple quantitative measure was sought which could describe the relationship between reflex coupling in the spinal cord of salamanders and the peripheral innervation fields of the nerves from which the reflexes were elicited.2. In decerebrate salamanders reflex responses were recorded between pairs of cut hind limb nerves. The latencies (S/R times) of these reflex responses were bilaterally symmetrical for a given pair of nerves and were shorter when the stimulated nerve of the pair had a large motor and sensory peripheral limb innervation field; this was especially obvious for reflexes between 15th and 17th segmental nerves.3. After cutting or crushing the 16th nerve in adult salamanders, the adjacent 15th and 17th nerves sprouted collaterally to innervate denervated skin and muscle. There was apparently complete recovery of normal tactile reflexes and walking movements within a month.4. The operation did not affect the reflex response (S/R) times for nerve combinations on the unoperated side, which were not significantly different from those of normal animals with similar sized peripheral nerve fields. The unoperated side therefore represented the preoperative condition.5. In animals where one or both the 15th and 17th nerves had increased its innervation field size, the S/R times between them were significantly shorter on the operated side when the nerve with the enlarged field was stimulated. The degree of shortening was greatest for nerves showing the largest increase in peripheral field area.6. The S/R times between the 15th and 17th nerves were similar to those measured in normal animals in which the peripheral fields were of similar size to the enlarged fields in the operated animals. In a few cases where the increase in field size was considerable, the S/R time between the 15th and 17th nerves became as short as that between the 15th and 16th nerves on the control side.7. After removal of the 15th nerve, the 14th nerve sprouted into the trunk skin and muscle previously innervated by the 15th nerve and the 16th nerve into denervated limb skin and muscle. In spite of the increased peripheral fields of both these nerves, there was no change in the S/R times between them, or between any other pair of limb nerves on the operated side.8. The decrease in the S/R times between the 15th and 17th nerves was only observed where the stimulated nerve had increased its peripheral limb innervation field. The possible causes and significance of this shortening reflex response times are discussed in the context of an apparently functionally appropriate adaptation in the spinal cord.

Animals↗

Evidence for the involvement in the baroreceptor reflex of a descending inhibitory pathway.

1. The onset and time course of baroreceptor inhibition of pre- and post-ganglionic sympathetic reflex activity has been examined in the anaesthetized cat.2. The shortest time to the onset of inhibition of an intercostal evoked reflex response in cardiac and renal nerve was less than 90 msec following a rise in pressure in a carotid sinus blind sac, and around 55 msec following stimulation of the ipsilateral sinus nerve. The cardiac nerve response was completely inhibited before the renal nerve response.3. Because of the long delays in the somato-sympathetic reflex pathway it is argued that these minimum times will be much less than the real central delay of baroreceptor inhibition. These were estimated by adding on the central times for the somato-sympathetic reflexes to give latencies of 94-143 msec for the inhibition.4. A spinal sympathetic reflex was inhibited by 30-75% following a rise in pressure in a carotid sinus blind sac or sinus nerve stimulation. The minimum time for this inhibition was around 100 msec.5. The baroreceptor inhibition of the spinal sympathetic reflex was abolished following section of a restricted region in the dorsolateral part of the lateral funiculus of the cervical spinal cord.6. Both pre- and post-ganglionic reflexes could be inhibited when stimulating within three regions of the medulla oblongata. The latency to inhibition elicited from the ventromedial reticular formation was short, some 5-30 msec, whereas that elicited from a ventrolateral region or the mid line raphe nucleus was long, some 90-160 msec.7. The possibility is discussed that the baroreceptor inhibition of both the pre- and post-ganglionic reflexes examined in this study is occurring at the spinal level via a pathway from either the raphe nuclei or ventrolateral medulla.

Animals↗

Electrophysiological characteristics of renorenal reflexes in the cat.

1. Experiments were done in anaesthetized, paralysed and artificially ventilated cats to determine the fibre composition of renal nerves and to study the functional characteristics of reflex responses recorded in efferent renal nerves during electrical stimulation of contralateral and ipsilateral afferent renal nerves. 2. Renal nerves were found to contain three afferent fibre groups (Abeta, Adelta and C); the majority of these fibres reach the sympathetic chain through the least splanchnic nerve. Efferent sympathetic nerves to the kidney were found to originate from the greater, lesser and least splanchnic nerves through a synapse in the coeliac ganglion. 3. Two contralateral renorenal reflex responses were demonstrated during selective stimulation of renal afferent A and C fibres. The first (A renorenal reflex) was elicited by stimulation with trains of pulses at low voltage and high frequency (200 Hz), had an onset latency of approximately 100 msec and was followed by post-excitatory depression. The second (C renorenal reflex) was demonstrated by trains of pulses at high voltage and low frequency (20--30 Hz), had an onset latency of approximately 350 msec and was also followed by post-excitatory depression. 4. Ipsilateral renorenal reflexes with characteristics similar to the contralateral reflexes were also demonstrated. 5. Renorenal reflexes were abolished by destruction of the spinal cord and administration of nicotine sulphate (5--20 mg/kg, i.v.), but were not affected by bicuculline (0.4 mg/kg, i.f.). 6. The significance and the physiological role of these renorenal reflexes as well as their pathways within the central nervous system remain to be determined.

Animals↗

Adrenergic and opioidergic modulation of a spinal reflex in the decerebrated rabbit.

1. In the decerebrated and spinalized rabbit, electrical stimulation of the sural nerve evokes a short-latency reflex in the ipsilateral ankle extensor gastrocnemius medialis (GM) which is tonically suppressed by endogenous opioids. In the present study we have investigated the inhibitory influences affecting this reflex in non-spinalized, decerebrated rabbits. 2. In non-spinalized rabbits, the thresholds and latencies of the sural-GM reflex were significantly higher than in spinalized preparations. The opioid antagonist naloxone and the alpha-adrenoceptor antagonist idazoxan potentiated the reflex in both preparations. Naloxone was significantly more effective in spinalized rabbits whereas idazoxan had a much larger effect in non-spinalized animals. 3. When the spinal cord was sectioned in the presence of naloxone alone, the GM reflex always increased in size. An ipsilateral hemisection of the cord was as effective as total section in this respect. When the section was performed in the presence of idazoxan and naloxone, the response usually decreased in size. 4. The alpha 2-adrenoceptor agonist clonidine depressed the reflex in spinalized rabbits, an action that was reversed by idazoxan but not by naloxone. 5. These data show that in the decerebrated, non-spinalized rabbit, the sural-GM reflex is tonically suppressed by endogenous opioids, presumably acting at the segmental level, and by an ipsilateral descending pathway which involves an alpha-adrenoceptor-mediated synapse. Activity in this descending pathway masks the facilitatory effects of opioid antagonists on spinal reflexes in this preparation.

Adrenergic alpha-Antagonists↗

Dependence of autogenic and heterogenic stretch reflexes on pre-load activity in the human arm.

1. Subjects held their right arm in a horizontal plane. The angle of the elbow was 90 deg. They exerted forces in several directions in the plane of the arm, varying independently the pre-load torques about shoulder and elbow. We measured electromyographic (EMG) activity in several arm muscles in response to force perturbations which extended the shoulder, without changing the elbow angle. 2. The EMG activity in flexors of both shoulder and elbow showed reflex responses at short latency (approximately 25 ms). In all muscles the reflex activity increased with the pre-load activity of that muscle. 3. The short-latency reflex activity of m. brachialis, which was not stretched by the perturbations, was independent of the pre-load activity of the muscles acting over the shoulder. 4. From these results we conclude that the force resulting from the short-latency reflex, assessed from the EMGs, does not counteract the perturbations exactly. Having found that the short-latency reflex is dependent on the pre-load direction, we argue that this dependence makes the short-latency reflex suitable for correcting fast movements for misjudgements of load. 5. At longer latencies (greater than 50 ms) the direction of the force resulting from the reflex, assessed from the EMGs, was almost independent of the direction of the pre-load. In our experiment the force resulting from the long-latency reflex counteracted the perturbations quite well.

Arm↗

Ankle stiffness of standing humans in response to imperceptible perturbation: reflex and task-dependent components.

1. It has been demonstrated that subjects can alter the reflex stiffness of the elbow and wrist in response to imperceptibly slow perturbations applied through a complaint coupling. We used this technique to measure ankle stiffness in standing subjects as a means of examining reflex activity. 2. During unperturbed stance, a linear relationship between ankle torque and ankle angle is expressed as a load stiffness. The load stiffness predicted from a subject's measured physical dimensions corresponds closely with the value measured by standing the subject on a force platform. 3. Slow perturbations were applied at waist level, through a spring, to standing subjects. The perturbations caused sway similar in magnitude and rate to the sway of normal stance. Ankle stiffness was measured during the period when the perturbations were unperceived. The contribution to ankle stiffness of reflexes that use visual information was assessed by eye closure. The ability of reflexes based on sensory information from the legs to maintain upright posture was assessed when subjects balanced a load equivalent to their own body, in a situation where neither visual nor vestibular information could assist. Ankle stiffness was measured while the load was perturbed. 4. The results show that a simple mechanical model of stance predicts the torque-angle relationship at the ankle. This relationship determines the minimal ankle stiffness required to stand, and reflex muscle stiffness is a necessary component of this ankle stiffness. Visual, vestibular and lower limb sensorimotor reflexes each contribute to ankle stiffness; however, the local sensory reflexes alone are sufficient to stand. For responses to unperceived perturbations, standing subjects can alter their reflex ankle stiffness according to intentional set.

Ankle↗

Cutaneous inhibitory receptive fields of withdrawal reflexes in the decerebrate spinal rat.

1. The inhibitory cutaneous input to the withdrawal reflex pathways to single hindlimb muscles was investigated in decerebrate spinal rats (n = 53) using electromyography. 2. Withdrawal reflexes in the peronei, extensor digitorum longus and tibialis anterior muscles of the leg were strongly inhibited by conditioning mechanical, thermal (CO2 laser) and intracutaneous electrical stimulation of specific skin areas. By contrast, withdrawal reflexes in the biceps posterior-semitendinosus muscles of the thigh could only be weakly inhibited by conditioning skin stimulation. 3. Powerful inhibition of withdrawal reflexes in single lower leg muscles was elicited from the ipsilateral hindpaw plantar area, which would move towards the stimulation on contraction in the respective muscle. In addition, weak nociceptive inhibition was evoked from the corresponding skin areas on the contralateral hindlimb and, in some muscles, the tail. 4. The ipsilateral inhibitory and excitatory receptive fields of the withdrawal reflexes in single muscles overlapped somewhat. On stimulation of these transitional areas the reflex responses were preceded by a short-lasting inhibition. 5. Graded mechanical and thermal stimulation demonstrated prominent inhibitors effects from nociceptive receptors. Weak inhibitory effects were elicited by innocuous mechanical stimulation, suggesting a weak contribution from low threshold mechanoreceptors. Latency measurements indicated an inhibitory input from both myelinated and unmyelinated fibres. 6. In conclusion, the withdrawal reflex pathways receive a powerful nociceptive inhibitory input through spinal pathways. The movement-related organization of this input suggests that it serves to prevent inappropriate withdrawal reflexes.

Animals↗

Central 5-HT7 receptors are critical for reflex activation of cardiac vagal drive in anaesthetized rats.

5-Hydroxytryptamine (5-HT; serotonin)-containing neurones contribute to reflex activation of parasympathetic outflow in a number of species, but the 5-HT receptors mediating these effects have yet to be fully determined. The present experiments demonstrate that central 5-HT7 receptors are involved in the vagal bradycardia evoked during the cardiopulmonary reflex, baroreflexes and the chemoreflex, as well as other autonomic changes caused by these reflexes. The experiments examined the effects of the selective 5-HT7 receptor antagonists SB-269970 and SB-656104 on these reflexes. For the cardiopulmonary reflex, when compared to time-matched vehicle control experiments, intracisternal application of SB-269970 (30-300 microg kg(-1), i.c.) dose-dependently attenuated the evoked bradycardia. At the highest dose, SB-269970 also attenuated the reflex hypotension and sympathoinhibition. The structurally different 5-HT7 receptor antagonist SB-656104 (100 microg kg(-1), i.c.) similarly attenuated the reflex bradycardia and hypotension. SB-269970 (100 microg kg(-1), i.c.) also attenuated the bradycardias evoked by electrical stimulation of aortic nerve afferents and the baroreflex evoked by the pressor response to phenylephrine (3-25 microg kg(-1), i.v.). The gain of the baroreflex was also significantly attenuated (0.15 +/- 0.06 versus 0.34 +/- 0.06 ms mmHg(-1)). Finally, SB-269970 (100 microg kg(-1), i.c.) significantly attenuated both the bradycardia and sympathoexcitation evoked by the chemoreflex. These data indicate that central 5-HT7 receptors play an important facilitatory role in the reflex activation of vagal outflow to the heart.

Anesthesia↗

Recurrent inhibition of the bladder C fibre reflex in the cat and its response to naloxone.

Recurrent inhibition of the bladder C fibre reflex was studied in adult female cats anaesthetized with alpha-chloralose. Test reflexes were evoked by electrical stimulation of bladder Adelta and C afferents in the right pelvic nerve and were recorded from the proximal end of a small ipsilateral pelvic nerve branch, transected close to the bladder. Such test reflexes were consistently depressed by repetitive electrical stimulation of the contralateral bladder pelvic nerve (20 Hz, 20 s) at intensities sufficient to recruit axons of bladder preganglionic neurones. The inhibition could be evoked after transection of the left dorsal roots S1-S4 and the sympathetic supply to the bladder but was abolished by transection of the pelvic nerve central to the site of stimulation. Hence, it most likely involved central recurrent collaterals of antidromically activated bladder preganglionic neurones. The reflex suppression was quite considerable - maximal C fibre reflexes were reduced to a group mean of 25% (+/- 9% confidence interval) of their control size. The effect had a slow onset, requiring a few seconds of conditioning stimulation to be revealed, and was very long lasting (minutes). Naloxone (0.01-0.5 mg kg(-1) i.v.) abolished the recurrent inhibition of both the C fibre and Adelta bladder reflexes, while inhibition from afferents in the dorsal clitoris nerve remained unchanged. It is concluded that the segmental bladder C fibre reflex and the spino-ponto-spinal Adelta micturition reflex are both targets of recurrent inhibition from bladder parasympathetic preganglionic neurones and that the effect involves an enkephalinergic mechanism.

Animals↗

Motor neurone excitability in back muscles assessed using mechanically evoked reflexes in spinal cord injured patients.

OBJECTIVE: The clinical and functional assessment of back muscles in human spinal cord injury (SCI) has received little attention. The aim of this study was to develop a method to assess the level of a thoracic spinal cord lesion based on the reflex activation of back muscles. METHODS: In 11 control subjects and in 12 subjects with clinically complete thoracic SCI (T2-T12), either a spinous process or an erector spinae muscle was prodded to elicit short latency reflexes recorded electromyographically at the spinal level of stimulation. An electromagnetic servo, attached to a blunt probe, applied stimuli at a frequency of 1 Hz and amplitude of 3 mm. Two trials of 50 mechanical prods were conducted at each site. RESULTS: Reflexes were evoked in control subjects in 82% of trials when the spinous process was prodded, and in 80% of trials when the muscle was prodded. In contrast, reflexes in SCI subjects could be elicited in 90-100% of trials two segments either above or below the lesion. Reflex responses in control subjects had a mean (SEM) latency of 5.72 (0.53) ms when the spinous process was prodded, and 5.42 (0.42) ms when the muscle was prodded. In the SCI subjects, responses had slightly (but insignificantly) longer latencies both above and below the lesion to either stimulus. The amplitude of reflex responses, expressed as a percentage of the background EMG, was on average 2-3 times larger at the three vertebral levels spanning the lesion in SCI subjects than at sites above or below the lesion or at any level in control subjects. CONCLUSION: We propose that the size of these mechanically evoked reflexes may be useful in determining the level of thoracic SCI. Furthermore, the reflexes might provide a valuable tool with which to monitor recovery after an intervention to repair or improve function of a damaged spinal cord.

Adult↗

Human anal reflexes.

By perianal electrical stimulation and EMG recording from the external anal sphincter the anal reflex was constantly present in normal subjects. The latency decreased within certain limits with increasing stimulation to an average minimum latency of 50 ms (SD 10.5). There was no difference between the minimum latency in normal subjects and patients with suprasegmental lesions of the CNS. The latency may be prolonged in patients with lesion of the reflex arc. By stimulation over the posterior tibial nerve behind the medial malleolus a reflex reaction could be picked up constantly from the anal sphincter in normal subjects. This reflex had a longer latency but a lower threshold than the reflex reaction from the tibialis anterior muscle. The average minimum latency from the anal sphincter was 93 ms (SD 21.1) and from the tibialis anterior muscle 64 ms (SD 7.9). In the absence of the anal reflex it may be possible to localise the defect to the afferent or efferent parts of the reflex by using types of stimulation. Preliminary studies of spinal shock revealed a perianally elicited anal reflex in all cases, but also a response to peripheral stimulation in some of the cases, more frequently found in the anal sphincter than in the tibialis anterior muscle.

Anal Canal↗

Effects of fixation and optokinetic stimulation on vestibulo-ocular reflex suppression.

Suppression of the vestibulo-ocular reflex was assessed in normal subjects and patients with neurological disorders to determine the relative effects on suppression of a single fixation target and an optokinetic field. Subjects were rotated sinusoidally in yaw at varying frequencies of up to 0.5 Hz whilst seated in a Barany chair. A comparison was made between eye movements in darkness, those produced during fixation on a central target mounted to the chair, and eye movements during fixation on the target plus an "earth-fixed" or "chair-fixed" visual background. Presentation of a background produced only minimal effects on the suppression of the vestibulo-ocular reflex in normal subjects. In patients with impairment of fixation suppression, suppression of the vestibulo-ocular reflex was not improved after presentation of either form of optokinetic field. The results demonstrate that central fixation is the predominant requirement for suppression of the vestibulo-ocular reflex. This correlates closely with the ability to pursue. Although the optokinetic reflex generates following eye movements similar to pursuit, it cannot be used to mediate suppression of the vestibulo-ocular reflex in the absence of an intact pursuit system. The findings strengthen the view that the optokinetic reflex evolved to act in synergy with the vestibulo-ocular reflex in generating compensatory eye movements.

Adult↗

The tibialis anterior reflex in healthy subjects and in L5 radicular compression.

Phasic stretch reflexes were evoked in the tibialis anterior (TA) muscle, by tapping the dorsal side of the foot with a hand-held reflex hammer. The responses were recorded by means of surface electrodes. The TA reflex was examined in 70 healthy subjects and in 18 patients with L5 radicular compression. In 58 (83%) of the healthy subjects the reflex could be recorded bilaterally, in eight (11%) subjects no reflex was found on either side, and in four (6%) it was absent in one leg. Simultaneous recordings from the gastrocnemius-soleus showed that TA responses were not caused by volume conduction from that muscle. In the 18 patients with L5 radicular compression the TA reflex was absent on the affected side 13 times (72%) and present bilaterally in the other five cases. If asymmetry of the reflex (unilateral absence) is considered as a test for the presence of L5 radicular compression, the likelihood ratio for a positive test is 12.0, and for a negative test 0.3. The examination of the TA reflex is easily performed and can be useful in the diagnosis of L5 radicular compression.

Humans↗

Unmasking of the trigemino-accessory reflex in accessory facial anastomosis.

OBJECTIVE: To evaluate the possible blink reflex responses in facial muscles reinnervated by the accessory nerve. METHOD: Eleven patients with a complete facial palsy were submitted to a surgical repair by an accessory facial nerve anastomosis (AFA). In this pathological group, blink reflex was studied by means of percutaneous electrical stimulation of the supraorbital nerve and recording from the orbicularis oculi muscle. A control group comprised seven normal people and seven patients with a complete Bell's facial palsy; in this group, responses on the sternocleidomastoideus (SCM) muscles were studied after supraorbital nerve stimulation. RESULTS: All the patients with AFA showed a consistent degree of facial reinnervation. Ten out of the 11 patients with AFA showed reflex responses; in six, responses were configured by a double component pattern, resembling the R1 and R2 components of the blink reflex; three patients had an R1-like response and one patient showed a unique R2 component. Mean values of latencies were 15.2 (SD 4.6) ms for the R1 and 85.3 (SD 9.6) ms for the R2. In the control group, eight out of 14 people had evidence of reflex responses in the SCM muscles; these were almost exclusively configured by a bilateral late component (mean latency 63.5 (SD15.9) ms) and only one of the subjects showed an early response at 11 ms. CONCLUSION: The trigemino-accessory reflex response in the pathological group was more complex and of a significantly higher incidence than in the control group. These differences could be tentatively explained by a mechanism of synaptic plasticity induced by the impairment of the efferent portion of the reflex. This could unmask the central linking between the trigeminal and the accessory limbs of the reflex. The findings described could be a demonstration of neurobionomic function in the repairing process of the nervous system.

Accessory Nerve↗

Identification and characterization of the esophagoglottal closure reflex in a feline model.

To identify a suitable animal model and to delineate the neural pathway and target organs of the esophagoglottal closure reflex we studied three species. Study showed the existence of an esophagoglottal closure reflex in cats. The presence of this reflex could not be documented in the opossum. In monkeys, because of the inadequacy of the available recording devices, its presence could not be ascertained. In the feline model, the closure response of the vocal folds to the abrupt generalized and segmental distension of the esophagus was similar to that of the humans. Study findings indicate that among glottal adductor muscles at least interarytenoid and lateral cricoarytenoid muscles are involved as target organs of the esophagoglottal closure reflex. Decerebration did not change the frequency of glottal closure response to esophageal distension, supporting the notion that this reflex is completely under brain stem control. Bilateral cervical vagotomy abolished the glottal closure induced by esophageal distension indicating that this reflex is mediated by the vagus nerve. Upper esophageal sphincter (UES) pressure response to esophageal distension by air was variable, suggesting that glottal and UES response to esophageal distension, although closely coordinated, are not dependent on one another. In summary, an esophagoglottal closure reflex exists in feline species, and many similarities in the elicitation and mediation of this reflex have been found with that of humans. This model could be used for further physiological studies.

Air↗

Effects of rectal distensions on nociceptive flexion reflexes in humans.

We previously showed that gastric distension inhibits the somatic nociceptive flexion RIII reflex. To explore further the viscerosomatic interactions, we tested in the present study the effects of rectal distensions on RIII reflexes. Rapid and slow-ramp rectal distensions were performed in 10 healthy volunteers with an electronic barostat. The RIII reflex was continuously recorded from the lower limb during both types of distension and from the upper limb during rapid distensions. The visceral sensations were scored on a graded questionnaire. Rapid distensions facilitated the RIII reflex recorded from the lower limb, but at the highest distension level, facilitation was followed by inhibition. Slow-ramp distension induced gradual inhibition of the RIII reflex, which correlated with both distension volume and visceral sensation. RIII reflex recorded from the upper limb was also inhibited by rapid rectal distensions. Reflex inhibitions were probably related to the activation of pain modulation systems. One plausible explanation for the facilitatory effects, observed only at the lower limb, is the convergence of rectal and reflex afferents at the same levels of the spinal cord. The differential effects of rapid and slow-ramp distensions suggest the activation of two distinct populations of mechanoreceptors by these two modes of distension.

Adult↗

Cardiac sympathetic afferent reflex in dogs with congestive heart failure.

It is well accepted that sympathetic tone is elevated in chronic heart failure (HF) and that the cardiac sympathetic afferent reflex is a sympathoexcitatory reflex. There have been no studies designed to examine the role of this reflex in control of sympathetic outflow in the HF state. In this study we tested the hypothesis that cardiac sympathetic afferent reflexes are enhanced in HF and are, therefore, capable of contributing to the increase in sympathetic outflow in this disease state. Ventricular pacing was carried out in 14 dogs until signs of HF were evident. Fourteen sham dogs served as controls. At the time of the acute experiment the dogs were anesthetized with alpha-chloralose. The hemodynamic [arterial pressure and heart rate (HR)] and renal sympathetic nerve activity (RSNA) responses to left ventricular epicardial application of two doses of bradykinin (BK) and capsaicin (Cap) were determined in the sinoaortic-denervated and vagotomized state. The MAP, RSNA, and HR responses to BK were greater in the HF group compared with the sham group. The RSNA response to BK (50 micrograms) in the HF group was significantly increased (34.0 +/- 5.9 vs. 11.5 +/- 4.2%, P < 0.05). The MAP, RSNA, and HR responses to Cap in the HF group were similar to the responses to BK. The RSNA response to Cap in the HF group was significantly increased (29.8 +/- 11.3 vs. 13.8 +/- 2.3% for 10 micrograms, P < 0.05 and 46.5 +/- 10.7 vs. 18.7 +/- 3.1% for 100 micrograms, P < 0.05). The cyclooxygenase blocker indomethacin (5 mg/kg i.v.) attenuated the reflex responses to BK in the HF group. These data suggest that the enhanced cardiac sympathetic afferent reflex to epicardial BK in HF appears to be mediated by altered levels of prostaglandin synthesis. Blockade of cardiac sympathetic afferents with topical lidocaine reduced baseline of RSNA significantly more in the HF state than in the normal state (-24.2 +/- 3.6 vs. -4.3 +/- 4.5%, P < 0.05). We conclude from these data that the cardiac sympathetic afferent reflex is sensitized in the HF state and speculate that this enhanced cardiac sympathetic afferent reflex may contribute to the sustained higher sympathetic tone in chronic HF.

Afferent Pathways↗

K+ channel blockade in the NTS alters efficacy of two cardiorespiratory reflexes in vivo.

We investigated the role of potassium conductances in the nucleus of the solitary tract (NTS) in determining the efficacy of the baroreceptor and cardiopulmonary reflexes in anesthetized rats. The baroreceptor reflex was elicited with an intravenous injection of phenylephrine to evoke a reflex bradycardia, and the cardiopulmonary reflex was evoked with a right atrial injection of phenylbiguanide. Microinjection of two Ca-dependent potassium channel antagonists (apamin and charybdotoxin) into the NTS potentiated the baroreceptor reflex bradycardia. This may reflect the increased neuronal excitability observed previously in vitro with these blockers. In contrast, the Ca-dependent potassium channel antagonists attenuated the cardiopulmonary reflex, whereas voltage-dependent potassium channel antagonists (4-aminopyridine and dendrotoxin) attenuated both the baro- and cardiopulmonary reflexes when microinjected into the NTS. The possibility that the reflex attenuation observed indicates a predominant distribution of certain potassium channels on gamma-aminobutyric acid interneurons is discussed.

4-Aminopyridine↗