Absence of respiration modulation of carotid sinus nerve inputs to nucleus tractus solitarius neurons receiving arterial chemoreceptor inputs

The reflex responses to activation of the arterial chemoreceptors are dependent upon when in the respiratory cycle the chemoreceptor stimulus is given. To determine if the respiratory modulation of the chemoreflex occurs within the nucleus tractus solitarius (NTS), intracellular recordings were obtained in pentobarbital-anesthetized, paralyzed and mechanically ventilated cats, from 22 non-respiratory NTS cells which were depolarized following activation of the ipsilateral carotid body chemoreceptors (by close arterial injection of <100 μ1 CO₂ saturated bicarbonate). Activation of the ipsilateral carotid body chemoreceptors evoked depolarizations with amplitudes of 2.9–4.6 mV and durations of 2.1–5.9 s. Three of these cells also received a convergent excitatory input from the carotid sinus baroreceptors. Carotid sinus nerve (CSN) stimulation evoked either an excitatory post-synaptic potential (EPSPs) (n = 14, 8 monosynaptic) or an excitatory/inhibitory sequence (EPSP/IPSPs) (n = 8, 1 monosynaptic). CSN evoked PSPs were separately averaged (25–50 sweeps) during periods of phrenic nerve activity and phrenic nerve silence and during periods when the lungs were inflated and when the lungs were deflated. No parameter of the CSN evoked PSPs (latency, peak amplitude, duration) was altered during periods of phrenic nerve activity or lung inilation (all P values > 0.12, Wilxocon signed-rank test). The results suggest that there is no respiratory modulation of arterial chemoreceptor inputs by either central respiratory drive or lung stretch receptor afferent inputs at this early stage of the reflex arc.     

Cerebellar haemorrhage as a cause of neurogenic pulmonary edema-case report

The neurogenic pulmonary edema is a rare clinical situation caused by an imbalance characterized by an excessive sympathetic outflow. It is observed mostly in young patients, is associated with brain or spinal cord haemorrhage, trauma, tumours or infections and is usually fatal. A case of neurogenic pulmonary edema in a 27-year-old woman is presented, caused by a cerebellar haemorrhage due to a vermian and paravermian arteriovenous malformation rupture. The vermian and hemispheric haemorrhage injuring the sub-lobule IX-b of the uvula induced a disruption of both carotid baroreceptor and chemoreceptor reflexes control mechanisms. Medical treatment with controlled ventilation, PEEP, diuretics and morphine reverted the pulmonary edema. After surgical treatment of the haemorrhage and cerebellar AVM the patient recovered to an almost normal social and professional life. The cerebellar lesion induced a temporary vermian sub lobule IX-b dysfunction that was responsible for the sympathetic storm that evoked the neurogenic pulmonary edema.     

Modulation of emetic response by carotid baro- and chemoreceptor activations

We hypothesized that baroreceptor or chemoreceptor activation might be involved in the emetic, and prodromal cardiovascular and respiratory responses. To test this hypothesis, we induced the emetic responses by gastric distension in anesthetized Suncus murinus (house musk shrew), that had intact and absent baroreceptor and chemoreceptor afferents. Secondly, we stimulated the aortic depressor nerve (ADN) and the carotid sinus nerve (CSN) with or without gastric distension. Internal carotid artery ligation in the bifurcation area, which abolished reflex bradycardia by baroreceptor activation, and abolition of chemoreceptor reflex bradycardia and hyperventilation, by carotid body denervation, suppressed the emetic response but did not abolish it. ADN denervation, which produced no significant effects on the baroreceptor or chemoreceptor reflex bradycardia, had no effect on the emetic response, including the prodromal phase. CSN stimulation with gastric distension elicited retching accompanied by reflex bradycardia and hypotension during or just after stimulation, whereas ADN stimulation with gastric distension did not induce the cardiovascular reflex, and had no effects on the emetic response. These results indicate that carotid, rather than aortic, baroreceptor or chemoreceptor activation plays an important role in the augmentation of cardiac parasympathetic activity and the development of emetic response. In conclusion, carotid baroreceptor or chemoreceptor activation, which is non-emetic stimulation, acts as a modulator in the central mechanisms of emesis.     

Actions of carotid chemoreceptors on subretrofacial bulbospinal neurons in the cat.

Thirty-one barosensitive bulbospinal neurons were recorded from the subretrofacial (SRF) nucleus in eight chloralose-anaesthetised, paralysed cats. Close arterial injections of CO2-saturated saline were used to stimulate carotid body chemoreceptors. Seven neurons were abruptly excited and six neurons abruptly inhibited by chemoreceptor stimuli: these were primary responses, independent of changes in blood pressure or central respiratory drive (monitored from the phrenic nerve). A further eight neurons responded only indirectly to chemoreceptor stimuli, showing enhanced modulation of their activity coupled to the enhanced central respiratory drive. The distinction between primary and secondary responses was shown more clearly when central respiratory drive was inhibited by superior laryngeal nerve stimulation. The remaining ten neurons showed no clear response to chemoreceptor stimuli. SRF bulbospinal neurons thus show the same range of responses to chemoreceptor stimuli as the sympathetic neurons they are believed to drive.     

Sympathetic influence on carotid chemoreceptor response to substance P in the cat.

Previous studies have suggested that substance P (SP) may play a role in the carotid chemoreceptor response to hypoxia. Given the data from these studies we speculated that within the carotid body hypoxia might release SP which then acts on the chemosensitive unit. Concomitantly SP might be released in the superior cervical ganglion (SCG) and increase sympathetic outflow to the carotid body by interacting with acetylcholine in the SCG. The resulting vasoconstriction in the carotid body would further increase neural output from the carotid body. Hence we hypothesized that the exogenous SP on the carotid chemoreceptor neural activity would decrease after eliminating preganglionic inflow into the SCG. The hypothesis was tested using anesthetized, paralyzed and artificially ventilated cats. Neural activity from the carotid body (carotid chemoreceptor activity) or from the SCG (ganglioglomerular efferent nerve activity (GGN)) was measured. Close intra-arterial administration of SP (10 micrograms) caused a sustained stimulation of the carotid chemoreceptor activity which was accompanied by a fall in arterial blood pressure. The magnitude and time-course of the carotid body responses were extremely variable among the cats. The duration of increased chemoreceptor activity was significantly shortened after a transection of the cervical sympathetic nerve (CVSN). As a control, the duration of carotid body stimulation produced by the second injection of SP in a group of sham-operated cats was measured. This was essentially the same as the first injection, suggesting that the tachyphylactic effect of SP was negligible. The effects of the commonly used pharmacological agents (nicotine, cyanide, dopamine) on carotid chemoreceptor activity were not affected by the transection of the CVSN, GGN activity was also increased by exogenous SP. These results suggest that the effect of exogenous SP on carotid chemoreceptor activity consists of two components: (1) an initial direct excitatory effect; (2) a slowly developing excitatory effect mediated by the sympathetic outflow to the carotid body. The effects could be augmented by the accompanying hypotension.     

Split medulla preparation in the cat: arterial chemoreceptor reflex and respiratory modulation of the renal sympathetic nerve activity

The study was undertaken in order to assess the changes in sympathetic output in a split medulla preparation of the cat which, as shown earlier, has impaired respiratory rhythm generation. The effects of medullary midsagittal sections on renal sympathetic nerve firing were investigated in chloralose anesthetized, paralyzed and artificially ventilated cats. Recordings of phrenic and recurrent laryngeal nerve activity served as indices of central respiratory rhythm generation. Sections, 5 mm deep from the dorsal medullary surface and extending 6 mm rostrally and 3 mm caudally to the obex, did not produce any significant changes in heart rate, blood pressure or tonic renal sympathetic nerve firing levels. They decreased or abolished, however, the respiratory rhythmicity in renal sympathetic nerve which paralleled the reduction of inspiratory discharges in phrenic and recurrent laryngeal nerves, and abolished the carotid body chemoreceptor-sympathetic reflex. The inspiratory activity remaining after the sections could still be enhanced by chemoreceptor stimulation. The inhibitory baroreceptor and pulmonary stretch receptor sympathetic reflexes, and the central excitatory effect of CO2 on renal sympathetic nerve firing were not altered. The effects of electrical stimulation within the midsagittal plane of the medulla have shown that descending pathways from the medullary inspiratory neurons (or their medullary collaterals) do not participate in the facilitation of spinal preganglionic neurons during inspiration and in relaying the pulmonary stretch receptor inhibitory sympathetic reflex. A region located close to the obex was identified from which excitatory responses in renal sympathetic nerves, compatible with the response obtained by carotid sinus nerve stimulation, could be evoked. It is concluded that a lesion in the midline of the lower medulla at the level of the obex selectively destroys cells or pathways which relay the carotid body chemoreceptor-sympathetic reflex.     

Responses of rostroventrolateral medulla spinal vasomotor neurones to chemoreceptor stimulation in rats

The activity of spinal projecting 'vasomotor' neurones of the rostroventrolateral medulla (RVL) has been recorded in anaesthetised and paralysed rats. They responded to carotid body chemoreceptor stimulation (0.208 M NaH2PO4) with an increase in discharge that preceded an evoked increase in arterial blood pressure. This initial excitatory response was followed by a fall in discharge correlated to the rise in blood pressure. RVL neurones, which had equivalent sensitivity to baroreceptor inputs but no spinal projecting axons, failed to exhibit the initial excitatory response on chemoreceptor stimulation. These observations suggest that the pressor response to chemoreceptor stimulation is mediated, at least partially, by excitation of RVL-spinal 'vasomotor' neurones.     

The influence of lobule IX of the cerebellar posterior vermis on the baroreceptor reflex in the decerebrate rabbit

Stimulation of lobule IX (the uvula) of the cerebellar posterior vermis, either electrically or chemically, has been shown to evoke marked cardiovascular effects in both rabbit and cat. Recent experiments suggest that this stimulation can also reduce the responsiveness of neurons in the nucleus tractus solitarii to baroreceptor inputs. The aim of the present study was thus to determine whether the uvula exerts an influence on the baroreceptor reflex. In order to evoke a reflex bradycardia in decerebrate rabbits, blood pressure was increased by inflating a Swan-Ganz catheter positioned in the descending aorta, and in some rabbits the aortic nerve was also stimulated electrically. In most rabbits, following uvula removal, significantly larger reflex falls in heart rate were observed. In a second group of rabbits, a lesion of cerebellar lobules VI-VIII had no effect on reflex bradycardia. It is concluded that the uvula tonically depresses the cardioinhibitory component of the baroreceptor reflex in the rabbit. The possible functional implications of these results are discussed.     

Effect on urinary bladder function and arterial blood pressure of the activation of putative purine receptors in brainstem areas

The effect on bladder function and arterial blood pressure of adenosine-5'-triphosphate (ATP) and its synthetic analogue, alpha,beta-methylene ATP (alpha,beta-meATP) applied by microinjection to brainstem areas was assessed in the anaesthetised, paralysed and artificially ventilated female rat. Recordings of bladder pressure, changes in the pelvic nerve activity, arterial blood pressure and heart rate were evaluated. The purinergic drugs were microinjected into two brainstem areas the periaqueductal grey matter (PAG) and the area of the Barrington nucleus/locus coeruleus (LC) - only after electrical stimulation (50 Hz, 1 ms, 30-50 microA; n(PAG) = 17; n(LC) = 18) and the microinjection of glutamate (2 mM, pH 7.4+/-0.1; n(PAG) = 16; n(LC) = 16) had shown increases of bladder pressure and/or rate of bladder contractions and/or pelvic nerve activity at specific sites. Electrical and glutamate activation of PAG evoked an increase of arterial blood pressure. Microinjections of ATP (20 mM, pH 7.4+/-0.1; n(PAG) = 11; n(LC) = 11) and alpha,beta-meATP (2 mM, pH 7.4+/-0.1; n(PAG) = 10; n(LC) = 9) both evoked consistent increases of bladder pressure and/or pelvic nerve activity. Stimulation with ATP elicited a biphasic change of arterial blood pressure characterised by an increase followed by a decrease which was accompanied by a rise of heart rate. Microinjection of alpha,beta-meATP into PAG did not elicit a consistent response: a decrease of arterial blood pressure was evoked in five rats, while in two other rats an increase occurred. Electrical stimulation and glutamate activation of Barrington's nucleus/LC evoked an increase of arterial blood pressure, but a decrease was observed after microinjection of both ATP and alpha,beta-meATP. At some sites (n = 8) the effect of alpha,beta-meATP after a pre-injection at the same site of the P2 purino receptor antagonist, suramin (20 mM, pH 7.4+/-0.1) was smaller than the control. At three sites within PAG and two within LC located more medially to sites where an excitatory response had been observed, electrical stimulation evoked a small decrease or no change in bladder pressure. Following the stimulus, a rise in bladder pressure was preceded by an increase of pelvic nerve activity. A similar effect of glutamate was observed in one case. These data suggest that activation of P2 purine receptors in both PAG and Barrington's nucleus/LC is implicated in the neuronal mechanisms that generate patterns of activity in the parasympathetic innervation of the bladder and that purines also act at this level to modify sympathetic outflow to the cardiovascular system.     

Inhibition of arterial baroreceptor and chemoreceptor reflex responses by neuropeptide Y in anaesthetised dogs.

The effects of bolus intravenous injections of neuropeptide Y (NPY) on increases in pulse interval (PI) evoked reflexly by arterial chemoreceptor and baroreceptor stimulation were investigated in anaesthetised dogs. The arterial chemoreceptors were stimulated by rapid injections of small volumes of CO2 into the carotid sinus or brief episodes of tracheal occlusion. Intravenous injections of NPY produced a prolonged attenuation of the reflex prolongation of PI induced by both methods. Two methods of testing the arterial baroreceptor reflex were used: steady-state increases in PI evoked in response to maintained step increases in systolic arterial blood pressure (SABP) from inflation of an aortic balloon-tipped catheter, and beat-by-beat increases in PI evoked reflexly by 'ramp' increases in blood pressure caused by intravenous injections of phenylephrine. In both methods the relationship between SABP and PI is linear over the range tested (up to SABP 200 mmHg), the slope of the line indicating the sensitivity of the reflex response. Intravenous injections of NPY produced a prolonged attenuation of the baroreceptor-cardiodepressor reflex measured by both methods. No significant differences were observed between the NPY-mediated inhibition of the direct effects on PI of electrical stimulation of a vagus nerve, and its inhibition of the reflex responses of PI to chemoreceptor or baroreceptor stimulation. The results indicate that the attenuation of reflex PI responses to arterial chemoreceptor and baroreceptor stimulation following an intravenous injection of NPY can be accounted for in terms of the action of NPY on vagal nerve endings at the heart, although additional sites of action cannot be ruled out.     

AMPA/kainate receptors mediate sympathetic chemoreceptor reflex in the rostral ventrolateral medulla

Previous studies have reported that information from carotid chemoreceptors activates sympathetic premotor neurons in the rostral ventrolateral medulla (RVLM) exclusively viaN-methyl-d-aspartic acid (NMDA) receptors. In this study, we examined the possible involvement of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/kainate receptors in the RVLM on sympathetic chemoreceptor reflex in pentobarbitone anaesthetised, vagotomised and artificially ventilated rats. Carotid chemoreceptor stimulation with brief N₂ inhalation increased splanchnic sympathetic nerve activity and arterial pressure in animals that had received an intravenous injection of the non-competitive NMDA receptor blocker, MK-801 (2 mg/kg). RVLM sympathetic premotor neurons could also be activated by brief hypoxia in the presence of MK-801. However, microinjection of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, a selective AMPA/kainate receptor antagonist, 2 mM, 100 nl) into the RVLM after intravenous MK-801 abolished the hypoxia evoked sympathoexcitatory response. These results demonstrate that AMPA/kainate receptors in the RVLM are involved in the chemoreceptor reflex pathway.     

Effects of stimulation of the hypothalamic paraventricular nucleus on blood pressure and renal sympathetic nerve activity

Effects of electrical and chemical stimulation of the paraventricular nucleus (PVN) of the hypothalamus on blood pressure were examined in rats anesthetized with urethane-chloralose. Focal electrical stimulation (10-25 microA, 50 Hz, 0.5 msec) within the PVN consistently decreased blood pressure. Microinjection of L-glutamate (0.5 M, 80 n1) into the PVN led to a decrease in blood pressure, while the same amount of saline injection had no effect. The depressor response was not affected by cervical vagotomy. In order to obtain direct evidence for involvement of sympathetic nerve activity in the PVN-induced depressor response, effects of PVN stimulation on renal sympathetic nerve activity were examined. Low intensity electrical stimulation of the PVN inhibited renal sympathetic nerve activity, whereas the high intensity stimulation evoked a transient excitation followed by long lasting inhibition in renal sympathetic nerve activity. Latencies of the inhibitory and the excitatory responses were about 200 msec and 50-100 msec, respectively, judged by peristimulus time histograms. The result suggests that activation of PVN neurons produces a decrease in blood pressure due to inhibition of sympathetic outflows.     

Cardiovascular control by medullary surface chemoreceptors

The cardiovascular and respiratory effects of superfusion of the ventral surface of the medulla with acid hypercapnic or alkaline hypocapnic solutions have been studied in anaesthetized, paralyzed, artificially ventilated cats. Peripheral chemoreceptor and baroreceptor denervation was achieved by section of carotid sinus, aortic and cervical vagus nerves. Systemic arterial and central venous pressure, hindquarters blood flow, heart rate and phrenic nerve activity were recorded. Acid hypercapnic (pH 6.8, pCO2 85 mm Hg) superfusion caused increases in systemic arterial pressure, phrenic nerve activity and heart rate, and a decrease in hindquarters blood flow. Alkaline hypocapnic (pH u.i, pCO2 less than 10 mmHg) superfusion caused opposite effects. These experiments indicate a significant role of the chemoreceptors of the ventral surface of the medulla in cardiovascular control.     

Interactive responses to stimulation of the amygdaloid central nucleus and baroreceptor afferent activation in the rabbit

Recent evidence suggests that the amygdaloid central nucleus (ACE) may contribute to the regulation of arterial baroreceptor-vagal reflex sensitivity. To obtain additional data relevant to this suggestion, interactions between stimulation of the ACE and arterial baroreceptor afferent activation were examined. New Zealand rabbits were anesthetized with alpha-chloralose and a stimulating electrode was implanted stereotaxically in the ACE. In the first series of experiments, cardiovascular responses to stimulation of the ACE were assessed during periods in which blood pressure was decreased using sodium nitroprusside or increased in the rostral arterial compartment by inflating the tip of a Swan-Ganz catheter positioned in the descending aorta. It was found that the magnitude of bradycardia to stimulation of the ACE was correlated with the level of arterial blood pressure at the onset of stimulation, such that higher blood pressures were associated with larger bradycardic responses. These data suggest that arterial baroreceptor afferent activity may be an important factor in the elicitation of bradycardia from the ACE. In the second series of experiments, the aortic nerve was isolated, and cardiovascular responses to stimulation of the aortic nerve and to low frequency (5 Hz) stimulation of the ACE were assessed both alone and in combination. Stimulation of the aortic nerve during low frequency stimulation of the ACE was found to produce bradycardia of a significantly larger magnitude than the sum of the responses produced by each stimulus presented alone. These data demonstrate that bradycardia to stimulation of baroreceptor afferent fibers is augmented significantly during low frequency stimulation of the ACE. Taken together, these results are consistent with the notion that the ACE may contribute to the sensitivity of the arterial baroreceptor-vagal reflex.     

Effects of baroreceptor activation on spontaneous activity in the sweat glands and nictitating membrane of the cat

(1) In chloralose-anesthetized cats, elevation of carotid sinus pressure caused blood pressure, sweat gland potentials and nictitating membrane tension to decrease. (2) The onset and recovery of the sweat gland and nictitating membrane responses usually preceded the respective phases of the blood pressure (depressor) response; the latencies of the sweat gland and nictitating membrane responses agreed with the latencies predicted for neural reflex pathways. (3) The sweat gland and nictitating membrane responses were evoked less consistently than the depressor response. (4) In experiments where only the sweat gland potentials and blood pressure were studied: (a) the sinus pressure threshold for inhibition of sweat gland activity was similar to the threshold for the depressor response; (b) cutting the sinus nerves, or blocking the efferent neural activity to the sweat glands, eliminated the effects of sinus pressure elevation on the sweat gland potentials; (c) with carotid sinus pressure held constant, decreases in blood pressure, produced by stimulating the peripheral end of the vagus nerve, did not affect the sweat gland potentials. (5) These results indicate that baroreceptors can reflexly modulate activity in sympathetic neurons whose target organs are not fundamentally involved in blood pressure regulation.     

Salivary secretion elicited by activation of the parabrachial nuclei in the cat.

The lateral pontine tegmentum contains the parabrachial nuclei (NPB) which have been identified as a relay nucleus for cardiovascular, respiratory and gustatory systems, but their role in the regulation of these systems is not well understood. We examined the effects of electrical and chemical stimulation of the NPB on blood pressure, phrenic and hypoglossal nerve activity and salivary secretion. These variables were measured in eight anesthetized (alpha-chloralose/urethane, 30/150 mg/kg, n = 5) or decerebrate (n = 3) cats before, during, and after trains of electrical stimulation (1 ms pulse duration, 10 Hz 5 min train duration, currents as low as 10 microA) delivered unilaterally to NPB. Stimulation of the NPB elicited copious salivary secretion (1100 +/- 270 mg, mean +/- S.D.; P less than 0.001). Secretion was blocked completely by prior administration of atropine. The effects of the stimulus train on the respiratory and cardiovascular systems were variable and inconsistent even though short-latency responses of phrenic and hypoglossal nerve activities to single pulses were consistent. The short-latency response of phrenic nerve activity was biphasic, a decrease followed by an increase in activity; the response of hypoglossal nerve activity was monophasic, a transient increase in activity. Effects of electrical stimulation were replicated by the injection of an excitatory amino acid agonist (kainic acid) into the dorsolateral pons. Injection of 50 nl of 10 mM kainic acid into the NPB evoked salivary secretion, indicating that this response was elicited by stimulation of cell bodies in the region. In addition, chemical excitation increased breathing frequency, peak phrenic nerve activity, and blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)     

Inhibition of renal sympathetic nerve activity by electrical stimulation of the hypothalamic paraventricular nucleus in anesthetized rats

In an attempt to obtain direct evidence for involvement of sympathetic outflow in paraventricular nucleus (PVN)-induced depressor response, effects of electrical stimulation of the PVN on renal sympathetic nerve activity were examined in urethane-chloralose anesthetized rats. Low intensity stimulation of the PVN inhibited renal sympathetic nerve activity, whereas the high intensity stimulation evoked an excitation followed by long-lasting inhibition in renal sympathetic nerve activity. Latencies of the inhibitory and the excitatory responses were about 200 ms and 50-100 ms, respectively. The result suggests that a decrease in blood pressure induced by low intensity stimulation of the PVN is due to inhibiting the sympathetic outflow.     

Dominant role of aortic baroreceptors in the cardiac baroreflex of the rat in situ

The arterial baroreceptors detect changes in blood pressure and form the afferent limb of the baroreflex which acts to buffer changes in pressure through reciprocal regulation of the sympathetic and parasympathetic outflow. We have previously shown that the sympathetic and parasympathetic limbs of the baroreflex operate over different pressure ranges and hypothesised that these differences in regulation of heart rate and sympathetic activity could originate from the baroafferents. We tested this hypothesis using sequential baroafferent denervations in the decerebrate, arterially perfused rat preparation. We found that baroreflex control of heart rate is critically dependent upon the aortic arch afferents with relatively little contribution from the carotid sinuses. Indeed the baroreflex bradycardia was attenuated by 85% (n=7) when only one aortic depressor nerve was cut indicating a strongly synergistic interaction between aortic baroafferents. By contrast baroreflex sympathoinhibition was dependent on inputs from all four sites, and the stimulation of any single site could elicit robust sympathoinhibition. These findings were independent of the sequence of baroafferent nerve resection (n=15). Perfusion of the isolated carotid sinus (n=5) showed that it was possible to elicit baroreflex sympathoinhibition (and changes in vascular resistance) without any significant change in heart rate despite the use of strong stimuli (>100 mmHg) or repeated pulsatile stimuli. These results indicate fundamental differences in the responses elicited by stimulation of the afferents from the carotid and aortic barosensor sites and suggest that their actions within the nucleus of the solitary tract are functionally specified (sympathetic versus parasympathetic).     

Benzodiazepine-sensitive GABA(A) receptors in the commissural subnucleus of the NTS are involved in the carotid chemoreceptor reflex in rats

We studied the role of benzodiazepine (BDZ) receptors in the commissural subnucleus of the nucleus tractus solitarius (commNTS) in chemoreceptor reflex in urethane-anesthetized, pancronium-immobilized, artificially ventilated and bilaterally vagotomized rats. A BDZ agonist, diazepam (1-4 micromol/kg), administered intravenously reduced resting phrenic nerve activity (PNA) and blood pressure (BP). Stimulation of carotid chemoreceptors induced an increase in PNA and an increase in BP. Diazepam inhibited this chemoreceptor reflex. The effects of intravenous injection of diazepam (4 micromol/kg) on the chemoreceptor reflex were antagonized by microinjection of the BDZ antagonist flumazenil (100 pmol) into the commNTS. Microinjection of flumazenil (100 pmol) alone had no effect on the basal PNA and BP, and the chemoreceptor reflex. These results suggest that BDZ receptors are present in the carotid chemoreceptor reflex pathway in the commNTS and potentiate GABA(A) transmission.     

The functional subdivisions of the nucleus tractus solitarii of the cat in relation to the carotid sinus nerve reflex

The field potentials evoked by electrical stimulation of the afferent A delta fibers of the ipsilateral carotid sinus nerve (CSN) were surveyed in all the regions of the nucleus tractus solitarii of the cat (NTS responses). Pressor and inspiratory responses, like the CSN chemoreceptor reflex, are elicited by electrical stimulation of the site of the NTS responses in the rostral regions, the lateral portions of the intermediate regions and the commissure regions. On the other hand, depressor and apneic responses, like the CSN baroreceptor reflex, are elicited by electrical stimulation of the site of the NTS responses in the medial portions of the intermediate regions and the dorsal portions of the commissure regions.