Sympathoadrenal excitation and inhibition by lower brainstem stimulation in cats

Effects of stimulation of brainstem sites on hemodynamics and plasma catecholamine levels were assessed in cats under chloralose-urethane anesthesia. Pressor areas of the dorsal medulla (DM) and ventrolateral medulla (VLM) and the depressor area of the paramedian reticular nucleus (PRN) were stimulated electrically using a monopolar electrode, or chemically using sodium glutamate microinjection. Plasma levels of norepinephrine (NE) and epinephrine (EPI) were measured in caval blood above the adrenal veins. Electrical stimulation of the DM and VLM produced increases in blood pressure and in plasma NE and EPI levels that were enhanced after acute vagotomies. The NE and EPI responses were attenuated after acute, bilateral adrenalectomies, confirming augmented adrenomedullary secretion, whereas the pressor responses were intact. Injection of sodium glutamate into the same pressor regions of the DM or VLM also produced pressor responses and elevated plasma catecholamine levels, indicating that the responses resulted from activation of neuronal perikarya. Stimulation of the PRN attenuated pressor and catecholamine responses during stimulation of the DM and VLM. The results indicate that pressor responses during stimulation of the DM and VLM are due at least partly to activation of perikarya in these regions, are associated with but not dependent on adrenomedullary activation, and are enhanced after vagotomy; and that neurons of the PRN exert inhibitory modulation of the pressor and adrenomedullary responses during stimulation of VLM and DM.     

Homocysteic acid elicits pressor responses from ventrolateral medulla and dorsomedial medulla

In rats and cats anesthetized with alpha-chloralose and urethane, the pressor response and its relative reactivity were studied following microinjection of dl-homocysteic acid (DLH, 2 nmol in 40 nl of saline) into the dorsomedial medulla (DM) or the ventrolateral medulla (VLM). DLH, which excites only cell bodies of neurons but not fibers of passage, consistently produced pressor responses in DM and VLM in both cats and rats. The pressor effects elicited from VLM were more pronounced than those from DM. In cats, the most active areas for DLH were found in the rostral and midmedulla; the pons and caudal medulla were less active. The pressor responses from DM and VLM were augmented following bilateral vagotomy, persisted after sectioning of the carotid sinus and aortic depressor nerves, and after cauterization of the carotid bodies with phenol. The response induced by DLH was more apparent from VLM than that from DM. These pressor effects were evoked directly by activation of neurons in these two regions, and were not necessarily related to any homocysteate blockade of baroreceptor and/or chemoreceptor reflexes. These results suggest that in the medulla there reside at least two discrete pressor areas, DM and VLM containing neuronal perikarya.     

Activation of noradrenergic mechanism attenuates glutamate-induced vasopressor responses in the pons and medulla of cats in vivo.

1. Using anesthetized cats, the authors examined the noradrenergic modulation of the glutamate induced pressor and depressor responses in various brainstem areas, including pontine gigantocellular tegmental field (FTG), dorsomedial medulla (DM), rostral ventrolateral medulla (RVLM), and caudal ventrolateral medulla (CVLM). 2. Unilateral microinjection of L-glutamate (Glu, 3 nmol in 30 nL saline) into FTG, DM and RVLM produced an increase in systemic arterial pressure (SAP) and a decrease in heart rate (HR), while into CVLM produced decreases of SAP and HR. 3. Application of norepinephrine (NE) into the pressor areas (0.05 to 5 nmol) did not alter the resting SAP and HR, but significantly attenuated the Glu-induced pressor response with an order of potency: FTG > DM > RVLM. In the depressor CVLM, NE alone produced a dose-dependent decrease of resting SAP and HR, but did not affect the Glu-induced depressor responses. 4. The involvement of different adrenoceptor subtypes was further investigated by application of selective adrenoceptor agonists including phenylephrine (alpha1), clonidine (alpha2), and isoproterenol (beta). Responses to these agonists are similar to those elicited by NE, except that only alpha-adrenoceptor agonists could antagonize the Glu-induced pressor responses of the RVLM. 5. Our observations indicate that NE not only inhibits the pressor mechanisms in various brainstem areas but also elicits a direct depressor response in CVLM. These findings also suggest that NE acts more likely a neurotransmitter, rather than a modulator, in the CVLM.     

Coexistence of autonomic and somatic mechanisms in the pressor areas of medulla in cats.

The effects of electrical stimulation and microinjection of sodium glutamate (0.5 M) in the sympathetic pressor areas of the dorsal medulla (DM), ventrolateral medulla (VLM), and parvocellular nucleus (PVC) on the knee jerk, crossed extension, and evoked potential of the L5 ventral root produced by intermittent electrical stimulation were studied in 98 adult cats anesthetized with chloralose and urethane. During electrical and glutamate stimulation of these pressor areas, in addition to the rise of systemic arterial blood pressure marked inhibition of the spinal reflex was produced, indicating presence of neuronal perikarya responsible for these actions. Mild to moderate augmentation of spinal reflexes was also observed during brain stimulation but only in a few cases. The magnitude of the somatic effects among the pressor areas of the VLM, DM, and PVC subsequent to glutamate activation was about the same. Induced spinal reflex inhibition, independent from the baroreceptor and vagal influence, remained essentially unaltered after acute midcollicular decerebration. The inhibition was also observed in cats decerebellated 8-10 days in advance. The inhibition was not affected after bilateral electrolytic- or kainic-acid-induced lesions in the paramedian reticular nucleus (PRN). On the contrary, PRN-induced spinal reflex inhibition was attenuated after bilateral lesions in the DM or VLM. Data suggest that there coexists neuronal subpopulations in the VLM, DM, and PVC that can affect both the sympathetic pressor systems and spinal reflexes.     

Contribution between dorsal and ventrolateral regions of medulla oblongata in vasomotor function of cats

In cats anesthetized with alpha-chloralose and urethane, the medulla oblongata was explored with electrical and/or chemical stimulation for vasopressor actions. Chemical stimulation included semimicroinjection of sodium glutamate or microinjection of dl-homocysteic acid (DLH). The dorsal (DM), particularly its dorsomedial (DMM) portion, and the ventrolateral (VLM) regions were found to be most sensitive to both electrical and chemical stimulation. In between these two regions there was an area in the ventral portion of the gigantocellular and the parvocellular reticular nuclei that was sensitive to electrical and somewhat sensitive also to chemical stimulation. The responses to chemical stimulation indicate the existence of perikarya in these three areas for vasopressor actions. The most active response of VLM followed microinjection of DLH into the region of nu. paragigantocellularis lateralis (PGL) and subretrofacial nu. These responses were about 30% greater than those from DM where the most active area was found in the DMM region including the nu. and tractus solitarius. When an extensive area of VLM was lesioned bilaterally with kainic acid (KA, 1 micrograms/100 nl), the resting systemic arterial blood pressure (SAP) fell 42% and the pressor response on DM stimulation fell by more than 80%. In contrast, after similar KA bilateral destruction of DM the resting SAP fell 38% and the pressor responses from 67%. When only a limited area in the PGL/subretrofacial nu. of the rostral VLM (3-4 pressor sites, 1 mm apart) on one side was lesioned, the resting SAP remained unaltered while the pressor response on the ipsilateral DMM decreased 76%. On the other hand, when a similar smaller KA lesion (3-4 sites) was made in the DMM, although the resting SAP did not change, the pressor response on stimulation of the ipsilateral rostral VLM decreased 28%. Further lesioning of the contralateral DMM then decreased the rostral VLM pressor response 62% without much alternation in the resting SAP. Results of the present experiments are in accordance with our previous results that neuronal perikarya for vasopressor action exist not only in VLM but also in DM (18,34) with the function of VLM slightly predominant over DM. It seems highly possible that reciprocal innervation exists between DM and VLM, at least between DMM and the PGL/subretrofacial nu. region.     

Paramedian reticular nucleus--sympathetic inhibition in spontaneously hypertensive rats

The cardiovascular reactivity of various areas in the medulla related to sympathetic or parasympathetic activation, or to sympathetic inhibition, was compared in spontaneously hypertensive rats (SHR) and in normotensive rats Wistar-Kyoto (WKY) or Sprague-Dawley (SD). In SHR, which has an elevated resting systemic arterial blood pressure (SAP), the sympathetic pressor responses elicited from electrical stimulation of the dorsomedial medulla (DMM), parvocellular lateral nucleus (PVC) or ventrolateral medulla (VLM) were more profound than those in WKY and SD. The depressor and bradycardia responses elicited from electrical stimulation of the paramedian reticular nucleus (PRN) (which exerts both sympathetic and parasympathetic inhibitions) or from the area of the solitary nucleus/dorsomotor nucleus of vagus (NTS/DMV) (where stimulation leads to both parasympathetic activation and sympathetic inhibition) were also more intensive in SHR than in WKY and SD. The elicited pressor and depressor responses, however, were not significantly different between WKY and SD. Our results are consistent with previous findings (15) that in SHR an increased sympathetic activity of the pressor areas of medulla contributes to the pathogenesis of hypertension. Sympathetic inhibition (PRN and NTS/DMV areas) and parasympathetic activation (NTS/DMV area) from these areas, however, may not be critically involved.     

Somatic depressor reflexes: results of specific 'depressor' afferents' excitation or an epiphenomenon of general anesthesia and certain decerebrations?

In chloralose-urethane anesthetized cats and unanesthetized decerebrate cats graded electrical stimulation of the tibial nerve A-afferents was performed and the resulting changes in the tibial nerve compound action potentials, heart rate and systemic arterial pressure were recorded. Three subgroups of the tibial nerve A delta-afferents were distinguished and their excitability, conduction velocity and relation to the circulatory reflexes were characterized. Stimulation of the same A-afferents evoked only tachycardic reflexes in high-mesencephalic unanesthetized cats while both tachy- and bradycardic reflexes developed in anesthetized brain-intact cats. The volleys of A beta-afferents elicited depressor reflexes in 50% of anesthetized cats but were ineffective in the other anesthetized brain-intact cats and in all the unanesthetized decerebrate cats. In anesthetized cats, the volleys of two low-threshold subgroups of A delta-afferents evoked only depressor reflexes and volleys of high-threshold A delta-afferents evoked both depressor and pressor reflexes in dependence on the deepness of anesthesia. In unanesthetized cats, effects of A delta-stimulation depended on the level of decerebration, being exclusively pressor when the most high-threshold A delta-fibers were stimulated in high-mesencephalic cats, both pressor and depressor when only low-threshold subgroups of A delta-fibers were stimulated in these cats, and exclusively depressor in prebulbar cats. The dependence of the direction of reflex blood pressure changes on the level of decerebration and anesthesia is incompatible with the classical concept of the so-called somatic depressor afferents. Moreover, general anesthesia is shown to suppress and invert not only excitatory effects of spinal A-afferents' volleys on sympathetic vasoconstrictor and cardioaccelerator neurones but the inhibitory effects of these afferents' signals on the vagal cardioinhibitory neurones, too. Contrary to this concept, we regard the 'somatic depressor reflexes' and accompanying bradycardia not as a result of 'specific' afferents excitation, but as an epiphenomenon of general anesthesia and certain decerebrations. This hypothesis is founded: (1) on the results of electrophysiological investigations of somato-sympathetic and somato-vagal reflexes indicating the existence of parallel excitatory and inhibitory interneuronal pathways between the spinal afferents and sympathetic and vagal neurones; and (2) on the assumption of unequal sensitivity of these pathways to certain anesthetics.(ABSTRACT TRUNCATED AT 400 WORDS)     

Medullary pathways involved in cardiac sympathoexcitatory reflexes in the cat

Stimulation of cardiac sympathetic afferents evokes excitatory cardiovascular reflexes. However, the exact regions in the brain that integrate these reflexes have not been identified. Expression of c-Fos in the neurons provides a useful marker of the activated neurons. In the present study, we examined the response of c-Fos within the medulla of the cat to chemical stimulation of cardiac sympathetic afferents. After bilateral sinoaortic denervation and cervical vagotomy, we applied bradykinin (BK, 1-10 microg, n=7) six times to the anterior ventricular surface every 20 min. We observed consistent increases in blood pressure and heart rate while the vehicle for BK (0.9% saline, n=6) produced no responses. Ninety minutes after the end of the sixth treatment, transcardial perfusion was performed with 4% paraformaldehyde and the brainstem was harvested for immunohistochemical staining. Compared to the control animals, we noted Fos immunoreactive neurons in the nucleus of the solitary tract, lateral tegmental field, caudal and rostral ventrolateral medulla (VLM), and vestibular nucleus in the BK-treated cats (all P<0.05). Fos immunoreactivity was found in catecholaminergic neurons of the VLM. These findings indicate that the activated neurons in the medulla, especially in the VLM, are involved in integration of cardiac-cardiovascular sympathoexcitatory reflexes.     

Lateral hypothalamic and peripheral cardiovascular afferent inputs to ventrolateral medullary neurons

Experiments were done in chloralose anesthetized, paralyzed and artificially ventilated cats to identify single units in ventrolateral medulla (VLM) projecting directly to the intermediate gray (IG) region of the upper thoracic cord and responding to inputs from pressor sites in the anterior lateral hypothalamus (Hla) and carotid sinus (CSN) and aortic depressor (ADN) nerves. Forty-eight units were antidromically activated in VLM to stimulation of the IG at the level of T2. Of these 48 units, 15 (31%) were orthodromically excited by stimulation of the Hla with a mean latency of 15.8 +/- 2.1 ms. In addition, 8 of the 15 units responding to Hla stimulation were also excited orthodromically by stimulation of either the CSN or ADN or both. Of the remaining 33 units, 15 responded to stimulation of only the buffer nerves and 18 were unresponsive to the tested inputs. These results provide electrophysiological evidence for the existence of neurons in VLM which receive hypothalamic and buffer nerve inputs and suggest that the VLM plays a role in integrating and relaying cardiovascular afferent information from peripheral baroreceptors and chemoreceptors and from supramedullary centers to provide effector signals to spinal autonomic neurons involved in the control of the circulation.     

Differential effects on sympathetic nerve activities elicited by activation of neurons in the pressor areas of dorsal and rostral ventrolateral medulla in cats.

Changes of the nerve activity of the sympathetic renal and vertebral nerves were elicited by microinjection of sodium glutamate (50 nmol/100 nl) into the pressor areas of the dorsal (DM) and rostral ventrolateral medulla (RVLM) in cats under urethane-chloralose anesthesia. Animals were bilaterally vagotomized, artificially ventilated, and paralyzed with gallamine triethiodide. The vertebral nerve activity always increased when pressor responses were induced by DM or RVLM stimulation. However, the effects of medullary stimulation on the renal nerve activity were variable. Three types of renal nerve responses concomitant with the pressor responses were observed in either baroreceptor-intact or baroreceptor-denervated cats. They were: (1) augmentation (type I); (2) attenuation (type II); and (3) insignificant change (type III). Type I responses were often elicited by RVLM stimulation whereas type II responses were often elicited by DM stimulation. Findings suggested that neurons integrating these sympathetic nerve activities were not equally distributed in the pressor areas of DM and RVLM. This result supports the notion that neurons located in different pressor areas of the brainstem exert differential effects over different sympathetic nerve activities.     

Properties of ventrolateral medullary neurons that respond to muscular contraction.

Previous results from this laboratory have suggested that neurons in the ventrolateral medulla (VLM) modulate the pressor response to muscular contraction. The purpose of the present study was to determine 1) if VLM neurons with a discharge pattern related to sympathetic discharge and/or the cardiac cycle are stimulated during muscular contraction, 2) if the neurons activated by muscular contraction project to the intermediolateral columns of the spinal cord and 3) the location of glutamate immunoreactive neurons in the medulla. Single-unit responses of ventrolateral medullary neurons to hindlimb muscular contraction evoked by ventral root (L7 and S1) stimulation were recorded in one group of anesthetized cats. Computer analyses were performed to determine if the resting discharge of VLM neurons correlated temporally with sympathetic nerve discharge and/or the cardiac cycle. The discharge rate of 21 of 27 neurons which had a discharge related to sympathetic nerve activity increased during muscular contraction. Neurons in some of the experiments were tested for axonal projections to the intermediolateral nucleus (T2 or T5) of the spinal cord with antidromic activation techniques. The discharge pattern of 78% of the VLM neurons which were activated antidromically was related to the cardiac cycle or sympathetic nerve discharge. Most (92%) reticulospinal VLM neurons with cardiovascular related discharge were excited by muscular contraction. In a second set of experiments, glutamate immunoreactivity was demonstrated in neurons within an area overlapping the location of VLM neurons which were excited by muscular contraction. These findings suggest that reticulospinal neurons in the ventrolateral medulla which have a discharge pattern related to cardiovascular activity contribute to the pressor reflex evoked by muscular contraction. These neurons may utilize glutamate as a neurotransmitter.     

Cardiovascular responses to electrical stimulation of the bed nucleus of the stria terminalis

To determine whether the influence of the bed nucleus of the stria terminalis (BST) on cardiovascular function can be localized to specific cytoarchitectural areas within the BST, urethane (1.3 g/kg)-anesthetized male Sprague-Dawley rats were probed for cardiovascular reactive sites. Electrical stimuli (50 μa, 50 Hz, and a 0.5 ms pulse duration), delivered through stereotaxically placed glass semimicroelectrodes, were localized to the BST. Sham-stimulated animals served as controls. Stimulation sites were correlated with cytoarchitecturally distinct areas within the BST, and changes in mean arterial pressure (MAP) were subjected to statistical analysis. Systematically probing the BST for cardiovascular reactive sites showed a correlation between evoked responses and distinct cytoarchitectural areas. Stimulation of the me dial BST produced increases in MAP; stimulation of the lateral aspect of the BST produced decreases in MAP. Both pressor and depressor responses were evoked from the area ventral to the anterior commissure. Pressor responses were elicited from the area immediatley ventral to the anterior commissure, and depressor responses followed stimulation of an area more ventral. All subnuclei showed corroborating cardiovascular responses to 20–30 n1 microinjection of sodium glutamate. Taken together, these data provide substantial evidence to indicate that the BST, particularly at more rostral areas, consists of a medial pressor area, a lateral depressor area, and a ventral area with both pressor and depressor zone. © 1995 Wiley-Liss, Inc.     

Thermoregulatory responses of decerebrate and spinal cats

Cooling the spinal cord of the unanesthetized cat elicited shivering, piloerection, and vasoconstriction. A high-level decerebration abolished these effects. Lowering the decerebration to the level of the lower pons or medulla reinstated these responses to spinal cord cooling. In unanesthetized chronic spinal cats, cooling the spinal cord below the level of a T6 transection produced similar thermoregulatory effects limited to the hind limbs, although it was of less intensity and without piloerection. A high-level decerebration abolished shivering in the forelimbs to whole body cooling, while permitting shivering below the level of transection to spinal cord cooling. Lowering the level of decerebration to the lower pons or medulla reinstated shivering, vasoconstriction, and piloerection in the forelimbs. The data suggest that there is a region in the midbrain and upper pontine tegmentum which exerts tonic inhibition on lower regions in the lower pons, medulla, and spnal cord. When released from inhibition these lower regions are capable of facilitating thermoregulatory responses. Such an organization resolves contradictory reports on the abolition of thermoregulation after decerebration and answers the question of why spinal cord cooling produces shivering in spinal preparations but not in decerebrate preparations.     

Evidence for a serotonergically mediated sympathoexcitatory response to stimulation of medullary raphe nuclei

The cardiovascular role of serotonin (5-HT) containing neurons in the midline medullary raphe nuclei was studied in anesthetized cats. High frequency electrical stimulation of nucleus (n.) raphe (r.) pallidus, n.r. obscurus and n.r. magnus produced both pressor and depressor responses. Single shock stimulation of pressor sites produced an excitatory evoked potential of sympathetic nervous discharge (SND) recorded from the inferior cardiac nerve. Conversely, single shock stimulation of vasodepressor sites resulted in a computer-summed inhibition of SND. The mean conduction velocity in the sympathoexcitatory medullo-spinal pathway to sympathetic preganglionic neurons was calculated to be 1.24 m/s. The 5-HT antagonists methysergide and metergoline blocked the excitation of sympathetic activity evoked from medullary raphe nuclei. In contrast, these agents failed to alter the sympathoexcitatory response to electrical stimulation of lateral medulla pressor sites or the sympathoinhibitory response elicited by raphe stimulation. The 5-HT uptake inhibitor chlorimipramine increased the duration of the sympathoexcitatory response evoked from the raphe but not from the lateral medulla. Finally, mid-collicular transection did not effect the excitation of sympathetic activity elicited by stimulation of medullary raphe nuclei. These data suggest that serotonergic neurons in the midline medullary raphe nuclei provide an excitatory input to sympathetic neurons in the spinal cord.     

Effects of prolactin-releasing peptide microinjection into the ventrolateral medulla on arterial pressure and sympathetic activity in rats

Prolactin-releasing peptide (PrRP), originally isolated from the hypothalamus, is highly localized in the cardiovascular regions of the medulla, and intracerebroventricular administration of PrRP causes a pressor response. In the present study we investigated the cardiovascular effects of PrRP applied to functionally different areas of the ventrolateral medulla (VLM), and to the nucleus tractus solitarius (NTS) and the area postrema (AP). In urethane-anesthetized rats, microinjection of PrRP into the pressor area of the most caudal VLM, recognized as the caudal pressor area in the rat, elicited dose-dependent increases in mean arterial pressure, heart rate, and renal sympathetic nerve activity. In the same injection area, neither thyrotropin-releasing hormone, corticotropin-releasing hormone nor angiotensin II affected these baseline cardiovascular variables. On the other hand, microinjection of PrRP into more rostral parts of the VLM, i.e. the depressor area of the caudal VLM and the pressor area of the rostral VLM, as well as the NTS and the AP, had no effect on these cardiovascular variables. Immunohistochemical analysis in the medulla revealed that the cardiovascularly PrRP-responsive region contained PrRP-immunoreactive cell bodies and nerve fibers. These results suggest that the most caudal VLM is an action site of PrRP to induce a pressor response, which is mediated, at least partly, by the increase in sympathetic outflow.     

Cardiovascular effects produced by micro-injection of angiotensin-(1–7) on vasopressor and vasodepressor sites of the ventrolateral medulla

In this study, we determined the cardiovascular effects produced by micro-injection of the heptapeptided Angiotensin-(1–7) [Ang-(1–7)] into the rat ventrolateral medulla (VLM). Micro-injection of Ang-(1–7) into the rostral VLM and the caudal pressor area of the VLM produced significant increases in arterial pressure, comparable to that observed with micro-injection of Ang II. The changes in arterial pressure were associated with more variable changes in heart rate (HR) (usually tachycardia). On the other hand, micro-injection of Ang-(1–7) into the caudal depressor area induced decreases in arterial pressure and HR. The results suggest that, besides Ang II, Ang-(1–7) is involved in the mediation of the cardiovascular actions of the renin-angiotensin system in the VLM.     

Reflex effects evoked by stimulation of hypoglossal afferent fibers

In pentobarbitone-anesthetized cats, electrical stimulation of the central ends of the main trunks of transected hypoglossal nerves evoked vascular (pressor or depressor) reactions, mydriasis, slow and deep breathing, and reflex activation of laryngeal and facial muscles. Stimulation of the central end of the transected ramus descendens hypoglossi also provoked reflex contraction of cricothyroideus. These reflexes may be elicited also after intracranial section of hypoglossal nerve roots, but not after intracranial section of ipsilateral vagal roots. The above reflexes were abolished by acute section of the ipsilateral hypoglossonodosal branch, but they may be reproduced by electrical stimulation of the central end of this anastomotic branch between hypoglossal nerve and nodose ganglion. Stimulation of the central end of one transected hypoglossus evoked reflex efferent discharges in contralateral hypoglossus and contraction of contralateral tongue muscles. Stimulation of the central end of one transected hypoglossal end-branch inhibited efferent discharges in another end-branch. The crossed hypoglossohypoglossal reflex and the ipsilateral reflex inhibition were abolished by section of the hypoglossonodosal branch or vagal roots at the stimulated side. We conclude that reflexes evoked by stimulation of peripheral hypoglossal nerve in cats are mediated by afferent fibers directed to the nodose ganglion and entering the brain stem via vagal roots.     

Electrolytic lesions in the depressor area of the ventrolateral medulla of the rat abolish depressor responses to the aortic nerve stimulation

The pressor (VLPA) and the depressor (VLDA) areas in the ventrolateral medulla were identified with the microinjections of L-glutamate (1.77 nmol/site) in artificially ventilated, pentobarbital-anesthetized male Wistar rats. Electrical stimulation of the left or right aortic nerve (1-6 V, 10-40 pulses/s, 3 ms) produced usual depressor responses. Electrolytic lesions (2.5 mA for 30 s) were placed bilaterally in the VLDA. Lack of responses to subsequent microinjections of glutamate into the VLDA indicated that the lesions were complete. The function of the VLPA was not compromised because it continued to respond to microinjections of glutamate. Subsequent stimulation of the aortic nerves failed to elicit the usual depressor responses. These results confirm our earlier reports indicating that the VLDA is important in mediating the depressor component of the aortic baroreflex.     

Blockade of cholinergic receptors in the C1 area abolishes hypertensive response to opiates in the A1 area of the ventrolateral medulla

Opiate receptor stimulation by microinjections of a delta-receptor agonist, D-Ala2-D-Leu5-enkephalin (DADLE) into the caudal depressor (A1) area of the ventrolateral medulla produced a hypertensive response which was prevented as well as reversed by the blockade of cholinergic receptors in the rostral pressor (C1) area. These results suggest that the hypertensive responses to opiates in the A1 area are mediated via cholinergic mechanisms in the rostral C1 area of the ventrolateral medulla and acetylcholine may be the neurotransmitter released in the ventrolateral pressor area.     

Direct pathway from neurons in the ventrolateral medulla relaying cardiovascular afferent information to the supraoptic nucleus in the cat

In chloralose anesthetized cats experiments were done to electrophysiologically identify neurons in the ventrolateral medulla (VLM) which relay cardiovascular afferent information directly to the supraoptic nucleus (SON). Action potentials elicited antidromically by electrical stimulation of the SON were recorded from 69 histologically verified single units in the VLM. Single units responded with latencies corresponding to conduction velocities of 7.8 ± 0.6m/s. Of these units 26 were excited orthodromically by stimulation of the buffer nerves; 12 responded to stimulation of only the carotid sinus nerve, 7 responded to stimulation of only the aortic depressor nerve, and 7 responded to both buffer nerves. The axons of VLM units that responded to buffer nerves conducted at a significantly slower velocity than those of non-responsive units (5.7 ± 0.4and9.1 ± 0.8m/s, respectively). These data provide electrophysiological evidence of two different populations of VLM neurons which project directly to the SON, and suggest that the direct pathway from the VLM to the SON is involved in the release of vasopressin by SON neurons during activation of baroreceptor and chemoreceptor afferent fibers.