Biomedical subjects

E Colombari

Publications and source records attributed to E Colombari.

At least 19 recordsLinked to original sources

PubMed2005

The bradycardic and hypotensive responses to serotonin are reduced by activation of GABAA receptors in the nucleus tractus solitarius of awake rats.

We investigated the effects of bilateral injections of the GABA receptor agonists muscimol (GABA A) and baclofen (GABA B) into the nucleus tractus solitarius (NTS) on the bradycardia and hypotension induced by iv serotonin injections (5-HT, 2 microg/rat) in awake male Holtzman rats. 5-HT was injected in rats with stainless steel cannulas implanted bilaterally in the NTS, before and 5, 15, and 60 min after bilateral injections of muscimol or baclofen into the NTS. The responses to 5-HT were tested before and after the injection of atropine methyl bromide. Muscimol (50 pmol/50 nl, N = 8) into the NTS increased basal mean arterial pressure (MAP) from 115 +/- 4 to 144 +/- 6 mmHg, did not change basal heart rate (HR) and reduced the bradycardia (-40 +/- 14 and -73 +/- 26 bpm at 5 and 15 min, respectively, vs -180 +/- 20 bpm for the control) and hypotension (-11 +/- 4 and -14 +/- 4 mmHg, vs -40 +/- 9 mmHg for the control) elicited by 5-HT. Baclofen (12.5 pmol/50 nl, N = 7) into the NTS also increased basal MAP, but did not change basal HR, bradycardia or hypotension in response to 5-HT injections. Atropine methyl bromide (1 mg/kg body weight) injected iv reduced the bradycardic and hypotensive responses to 5-HT injections. The stimulation of GABA A receptors in the NTS of awake rats elicits a significant increase in basal MAP and decreases the cardiac Bezold-Jarisch reflex responses to iv 5-HT injections.

Animals↗

PubMed2005

Baroreflex function in conscious rats submitted to iron overload.

Our hypothesis is that iron accumulated in tissue, rather than in serum, may compromise cardiovascular control. Male Fischer 344 rats weighing 180 to 220 g were divided into 2 groups. In the serum iron overload group (SIO, N = 12), 20 mg elemental iron was injected ip daily for 7 days. In the tissue iron overload group (TIO, N = 19), a smaller amount of elemental iron was injected (10 mg, daily) for 5 days followed by a resting period of 7 days. Reflex heart rate responses were elicited by iv injections of either phenylephrine (0.5 to 5.0 microg/kg) or sodium nitroprusside (1.0 to 10.0 microg/kg). Baroreflex curves were determined and fitted to sigmoidal equations and the baroreflex gain coefficient was evaluated. To evaluate the role of other than a direct effect of iron on tissue, acute treatment with the iron chelator deferoxamine (20 mg/kg, iv) was performed on the TIO group and the baroreflex was re-evaluated. At the end of the experiments, evaluation of iron levels in serum confirmed a pronounced overload for the SIO group (30-fold), in contrast to the TIO group (2-fold). Tissue levels of iron, however, were higher in the TIO group. The SIO protocol did not produce significant alterations in the baroreflex curve response, while the TIO protocol produced a nearly 2-fold increase in baroreflex gain (-4.34 +/- 0.74 and -7.93 +/- 1.08 bpm/mmHg, respectively). The TIO protocol animals treated with deferoxamine returned to sham levels of baroreflex gain (-3.7 +/- 0.3 sham vs -3.6 +/- 0.2 bpm/mmHg) 30 min after the injection. Our results indicate an effect of tissue iron overload on the enhancement of baroreflex sensitivity.

Animals↗

PubMed2004

A low protein diet causes an increase in the basal levels and variability of mean arterial pressure and heart rate in Fisher rats.

The correlation between nutrition and cardiovascular related disorders is a well-established fact. Previous work from our Laboratory has suggested a significant compromise of cardiovascular reflexes in conscious rats submitted to a low-protein (LP) diet. Our working hypothesis is that the basal level of mean arterial pressure (MAP), variability of the mean arterial pressure (VMAP), heart rate (HR) and variability of heart rate (VHR) are altered in rats submitted to a protein restricted diet. Two experimental groups were used: control group (normal protein 15%, NP) and malnourished group (low-protein 6%, LP). In order to verify the efficiency of the dietary restriction we measured body weight, total blood protein, plasma albumin, urea and glucose. Our experiments demonstrated that the malnourished rats presented augment levels of basal MAP (LP 122+/-2 mmHg vs. NP 113+/-1 mmHg) and of VMAP (LP 12.8+/-1.5mmHg vs. NP 9+/-1mmHg) when compared to the control group. We observed similar increased levels, in the malnourished group, for both HR (LP 429+/-8 bpm vs. NP 381+/-7bpm) and VHR (LP 67.6+/-8.3bpm vs. NP 44.4+/-4.9bpm). Our results suggest a correlation between the LP diet in Fisher rats and the increased basal levels of mean arterial pressure, HR and their respective variability.

Animals↗

PubMed2001

Hemodynamic effects elicited by microinjection of glutamatergic agonists into NTS of conscious rats.

In this study, we characterized the arterial pressure, heart rate, and regional vascular conductance responses elicited by unilateral microinjection of ionotropic glutamatergic agonists N-methyl-D-aspartic acid (NMDA and non-NMDA) into the nucleus of tractus solitarius (NTS) of conscious rats. Microinjections of NMDA and S-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) caused changes in mean arterial pressure (MAP). Lower doses elicited decreases in MAP, whereas higher doses elicited biphasic responses (decreases followed by increases). Both agonists induced bradycardia and elicited dose-dependent vasoconstriction in the renal, mesenteric, and hindquarter beds. AMPA elicited delayed vasodilation in the hindquarter bed but NMDA did not. Bradycardia and initial hypotension produced by each agonist were abolished by systemic administration of the muscarinic antagonist methylatropine. However, methylatropine did not affect either the vasoconstriction or the vasodilatation. The contrasting hemodynamic effects produced by NMDA and AMPA could be caused by activation of differential subsets of NTS neurons. Preferential activation of one subset could produce the NMDA-related responses, whereas activation of another subset would elicit AMPA-related responses.

Animals↗

PubMed2001

Role of the medulla oblongata in hypertension.

Brain pathways controlling arterial pressure are distributed throughout the neuraxis and are organized in topographically selective networks. In this brief review, we will focus on the medulla oblongata. The nucleus tractus solitarius (NTS) is the primary site of cardiorespiratory reflex integration. It is well accepted that lesions or other perturbations in the NTS can result in elevations of arterial pressure (AP), with many of the associated features so commonly found in humans. However, recent studies have shown 2 distinct subpopulations of neurons within the NTS that can influence AP in opposite ways. Commissural NTS neurons located on the midline may contribute to maintenance of hypertension in spontaneously hypertensive rats (SHR), because small lesions in this area result in a very significant reduction in AP. Also involved in this blood pressure regulation network are 2 distinct regions of the ventrolateral medulla: caudal (CVLM) and rostral (RVLM). Neurons in CVLM are thought to receive baroreceptor input and to relay rostrally to control the activity of the RVLM. Projections from CVLM to RVLM are inhibitory, and a lack of their activity may contribute to development of hypertension. The RVLM is critical to the tonic and reflexive regulation of AP. In different experimental models of hypertension, RVLM neurons receive significantly more excitatory inputs. This results in enhanced sympathetic neuronal activity, which is essential for the development and maintenance of the hypertension.

Animals↗

PubMed2001

Lesions of the commissural nucleus of the solitary tract reduce arterial pressure in spontaneously hypertensive rats.

It has been suggested that increased sympathetic activity and arterial chemoreceptors are important for the high blood pressure in spontaneously hypertensive rats (SHR). Electrolytic lesions of the commissural nucleus of the solitary tract (commNTS) abolish (1) the cardiovascular responses to chemoreflex activation with potassium cyanide (KCN) in normotensive rats and (2) the hypertension that follows acute aortic baroreceptor denervation in rats. Therefore, in this study we investigated the effects of electrolytic lesions of the commNTS on basal mean arterial pressure (MAP), baroreflex, and chemoreflex in SHR and in normotensive control Wistar-Kyoto (WKY) and Wistar rats. CommNTS lesions elicited a dramatic fall in MAP to normal levels during the period of study (from the first to fourth day following lesions) in SHR and almost no changes in WKY and Wistar rats. The pressor responses to chemoreflex activation with KCN tested in the days 1 and 4 after commNTS lesions were abolished in SHR and in normotensive strains. The reflex tachycardia induced by sodium nitroprusside was also attenuated in days 1 and 4 after commNTS lesions in SHR, WKY, and Wistar rats. The data suggest that the integrity of commNTS is important for the maintenance of high blood pressure in SHR and for the reflex responses dependent on sympathetic activation either in SHR or in normotensive strains.

Animals↗

PubMed2000

Enhanced pressor response to carotid occlusion in commNTS-lesioned rats: possible efferent mechanisms.

Bilateral common carotid occlusion (BCO) over a period of 60 s in conscious rats produces a biphasic pressor response, consisting of an early (peak) and late (plateau) phase. In this study we investigated 1) the effects of lesions of the commissural nucleus of the solitary tract (commNTS) on the cardiovascular responses produced by BCO in conscious rats and 2) the autonomic and humoral mechanisms activated to produce the pressor response to BCO in sham- and commNTS-lesioned rats. Both the peak and plateau of the pressor response produced by BCO increased in commNTS-lesioned rats despite the impairment of chemoreflex responses induced by intravenous potassium cyanide. In sham rats sympathetic blockade with intravenous prazosin and metoprolol, but not vasopressin receptor blockade with the Manning compound, reduced both components of BCO. In commNTS-lesioned rats the sympathetic blockade or vasopressin receptor blockade reduced both components of BCO. The results showed 1) the sympathetic nervous system, but not vasopressin, is important for the pressor response to BCO during 60 s in conscious sham rats; 2) in commNTS-lesioned rats, despite chemoreflex impairment, BCO produces an increased pressor response dependent on sympathetic activity associated with vasopressin release; and 3) the increment in the pressor response to BCO in commNTS-lesioned rats seems to depend only on vasopressin secretion.

Adrenergic alpha-Agonists↗

PubMed2000

Afferent pathways in cardiovascular adjustments induced by volume expansion in anesthetized rats.

The role of baroreceptors, cardiopulmonary receptors, and renal nerves in the cardiovascular adjustments to volume expansion (VE) with 4% Ficoll (Pharmacia; 1% body wt, 0.4 ml/min) were studied in urethan-anesthetized rats. In control animals, VE produced a transitory increase in mean arterial pressure (MAP), which peaked at 10 min (17 +/- 4 mmHg) and increases in renal (128 +/- 6 and 169 +/- 19% of baseline at 10 and 40 min, respectively) and hindlimb vascular conductance (143 +/- 6 and 150 +/- 10%). These cardiovascular adjustments to VE were unaffected by bilateral vagotomy. After sinoaortic denervation, the increase in MAP induced by VE was greater than in control rats (30 +/- 4 mmHg). However, renal vasodilation in response to VE was blocked, whereas hindlimb vasodilation was similar to that observed in control rats. After unilateral renal denervation (ipsilateral to flow recording), the initial renal vasodilation was blocked. However, 40 min after VE, a significant renal vasodilation (125 +/- 4%) appeared. The hindlimb vasodilation and MAP responses were unaffected by renal denervation. These results demonstrate that the baroreceptor afferents are an essential component of cardiovascular adjustments to VE, especially in the control of renal vascular conductance. They also suggest that renal vasodilation induced by VE is mediated by neural and hormonal mechanisms.

Anesthesia↗

PubMed1999

Role of carbon monoxide in L-glutamate-induced cardiovascular responses in nucleus tractus solitarius of conscious rats.

Heme oxygenase degrades heme to form carbon monoxide. It has been reported that heme oxygenase-derived carbon monoxide may interact with L-glutamate (L-Glu) receptors in the nucleus tractus solitarius (NTS). Integrative studies suggest that heme oxygenase inhibitors raise blood pressure, in part, by inhibiting carbon monoxide formation in the NTS. The currents studies were designed to determine if heme oxygenase inhibitors affect the cardiovascular actions of L-Glu in the NTS. Accordingly, MAP and HR responses to unilateral microinjections of L-Glu (5 nmol/100 nl) into the NTS were measured before and after ipsilateral microinjections of zinc deuteroporphyrin 2,4-bis glycol (ZnDPBG, 4.5 nmol/100 nl) or chromium mesoporphyrin (CrMP, 1.5 nmol/100 nl) in awake rats chronically instrumented with NTS guide cannulaes and arterial catheters. With respect to non-treatment (+36+/-5 mmHg, -107 bpm, n=10), ZnDPBG pre-treatment attenuated the pressor and bradycardic responses to L-Glu (+7+/-3 mmHg, -10+/-6 bpm, P<0.05). CrMP similarly attenuated cardiovascular responses to L-Glu (+47+/-3 mmHg, -68+/-8 bpm vs. +20+/-5 mmHg, -40+/-9 bpm; before vs. after, n=10, P<0.05). Matched series yielded no vehicle- or time-related effects. Our findings suggest that a heme oxygenase product, such as carbon monoxide, may affect NTS glutamatergic neurotransmission to participate in cardiovascular control.

Analysis of Variance↗

PubMed1999

Carbon monoxide as a novel mediator of the febrile response in the central nervous system.

Heme oxygenase catalyzes the metabolism of heme to biliverdin, free iron, and carbon monoxide (CO), which has been shown to be an important neuromodulatory agent. Recently, it has been demonstrated that lipopolysaccharide (LPS) can induce the enzyme heme oxygenase in glial cells. Therefore, the present study was designed to test the hypothesis that central CO plays a role in LPS-induced fever. Colonic body temperature (T(b)) was measured in awake, unrestrained rats (basal T(b) = 36.8 +/- 0.2 degrees C). Intracerebroventricular injection of zinc deuteroporphyrin 2,4-bis glycol (ZnDPBG; 75 nmol), a heme oxygenase inhibitor, caused no significant change in T(b), indicating that the central heme oxygenase pathway plays no tonic role in T(b) under the experimental conditions used. Intraperitoneal injections of LPS (50-100 microgram/kg) evoked dose-dependent increases in T(b). Intracerebroventricular injection of ZnDPBG in febrile rats attenuated LPS-induced fever (thermal index with ZnDPBG = 1.1 +/- 0. 2 degrees C, thermal index with vehicle = 2.3 +/- 0.4 degrees C), suggesting that the central heme oxygenase pathway plays a role in fever generation. The antipyretic effect of ZnDPBG could be reversed by intracerebroventricular administration of heme-lysinate or CO-saturated saline. Collectively, our data indicate that CO arising from heme oxygenase may play an important role in fever generation by acting on the central nervous system.

Animals↗

PubMed1999

Commissural NTS lesions and cardiovascular responses in aortic baroreceptor-denervated rats.

Both acute (1 day) lesions of the commissural nucleus of the solitary tract (commNTS) and aortic baroreceptor denervation increase pressor responses to bilateral common carotid occlusion (BCO) during a 60-second period in conscious rats. In this study, we investigated the following: (1) the effects of commNTS lesions on basal mean arterial pressure (MAP) and heart rate (HR) of aortic denervated (ADNx) rats; (2) the effects of acute commNTS lesions on pressor responses to BCO in ADNx rats; and (3) the effects of chronic (10 days) commNTS lesions on the pressor response to BCO. ADNx increased basal MAP and HR in sham-lesioned rats. Acute commNTS lesions abolished the MAP and HR increases observed in ADNx rats. Acute commNTS lesions increased the pressor responses to BCO in rats with intact-baroreceptor innervation but produced no additional change in the pressor response to BCO in ADNx rats. Chronic commNTS lesions did not change the pressor responses to BCO in rats with intact-baroreceptor innervation. The data show that acute commNTS lesions abolish the MAP increase produced by aortic baroreceptor denervation. They also suggest that acute commNTS lesions enhance the pressor response to BCO by partial withdrawal of aortic baroreceptor inputs into the NTS. Chronically, reorganization in the remaining aortic baroreceptor or in the baroreflex function as a whole might produce normalization of the cardiovascular responses to BCO.

Animals↗

PubMed1999

Carbon monoxide: from toxin to endogenous modulator of cardiovascular functions.

Carbon monoxide (CO) is a pollutant commonly recognized for its toxicological attributes, including CNS and cardiovascular effects. But CO is also formed endogenously in mammalian tissues. Endogenously formed CO normally arises from heme degradation in a reaction catalyzed by heme oxygenase. While inhibitors of endogenous CO production can raise arterial pressure, heme loading can enhance CO production and lead to vasodepression. Both central and peripheral tissues possess heme oxygenases and generate CO from heme, but the inability of heme substrate to cross the blood brain barrier suggests the CNS heme-heme oxygenase-CO system may be independent of the periphery. In the CNS, CO apparently acts in the nucleus tractus solitarii (NTS) promoting changes in glutamatergic neurotransmission and lowering blood pressure. At the periphery, the heme-heme oxygenase-CO system can affect cardiovascular functions in a two-fold manner; specifically: 1) heme-derived CO generated within vascular smooth muscle (VSM) can promote vasodilation, but 2) its actions on the endothelium apparently can promote vasoconstriction. Thus, it seems reasonable that the CNS-, VSM- and endothelial-dependent actions of the heme-heme oxygenase-CO system may all affect cardiac output and vascular resistance, and subsequently blood pressure.

Blood Pressure↗

PubMed1998

Hemodynamic effects of L-glutamate in NTS of conscious rats: a possible role of vascular nitrosyl factors.

This study examined peripheral mechanisms responsible for changes in mean arterial blood pressure, heart rate, and renal, mesenteric, and hindquarter vascular resistances produced by microinjections of L-glutamate (L-Glu) into the nucleus tractus solitarii (NTS) of conscious rats. Microinjection of L-Glu produced an initial pressor response, bradycardia, and vasoconstriction in each vascular bed. Subsequent hindquarter vasodilation was observed. After prazosin was administered, L-Glu produced initial hypotension that was probably due to reduced cardiac output. This hypotension was followed by hindquarter vasodilation. Inhibition of nitric oxide synthesis did not affect the initial hypotension or bradycardia in rats treated with prazosin, but the first microinjection of L-Glu after administration of prazosin and NG-nitro-L-arginine methyl ester (L-NAME) produced significantly greater hindquarter vasodilation than after administration of prazosin alone. Second and third microinjections of L-Glu produced significantly smaller hindquarter vasodilation. We conclude that 1) hemodynamic effects produced by microinjection of L-Glu into the NTS of conscious rats involves activation of the sympathetic nervous system and 2) release of preformed nitrosyl factors may mediate vasodilation in the hindquarter vascular bed.

Animals↗

PubMed1997

NMDA receptor antagonist blocks the bradycardic but not the pressor response to L-glutamate microinjected into the nucleus tractus solitarius (NTS) of unanesthetized rats.

In the present study we evaluated the role of NMDA receptors on the pressor and bradycardic responses to L-glutamate (L-Glu) microinjected into the nucleus tractus solitarius (NTS) of unanesthetized rats. L-Glu (1 nmol/100 nl) was microinjected into the NTS before and 10 min after microinjection of phosponovaleric acid (AP-5), a selective NMDA receptor antagonist, into the NTS of three different groups of rats (0.5, 2.0 and 10.0 nmol/100 nl). Microinjection of AP-5 into the NTS produced a dose-dependent reduction in the bradycardic response to L-Glu. However, no significant change in the pressor response to L-Glu was observed. These results indicate that the activation of the cardiovagal component (bradycardia) by L-Glu involves NMDA receptors and suggest that the activation of the sympatho-excitatory component (pressor response) by L-Glu in the commissural NTS is mediated by non-NMDA receptors.

2-Amino-5-phosphonovalerate↗

PubMed1997

Role of endogenous carbon monoxide in central regulation of arterial pressure.

We investigated the contribution of neural mechanisms to the arterial pressure increase produced by zinc deuteroporphyrin 2,4-bis glycol (ZnDPBG), an inhibitor of endogenous carbon monoxide synthesis. The arterial baroreceptor reflex control of heart rate was examined in rats with and without ZnDPBG pretreatment (45 micromol/kg IP) by analysis of the arterial pressure-heart rate relationship during infusions of phenylephrine or sodium nitroprusside to vary arterial pressure. ZnDPBG increased arterial pressure from 110 +/- 3 to 126 +/- 2 mm Hg without eliciting bradycardia. The maximum gain of the heart rate response to changes in arterial pressure was attenuated by ZnDPBG treatment (-1.9 +/- 0.3 versus -4.8 +/- 1.0 bpm/mm Hg). The possibility that ZnDPBG elevates arterial pressure by attenuating baroreceptor reflex function was addressed by comparing the pressor response to ZnDPBG (45 micromol/kg IP) in rats with and without sinoaortic denervation. The pressor effect of ZnDPBG was similar in rats with and without arterial baroreceptor deafferentation, implying that the increase in pressure is not simply the consequence of attenuated baroreceptor reflex function per se. The possibility that ZnDPBG increases arterial pressure via an effect on the nucleus tractus solitarii (NTS) also was investigated. ZnDPBG (1 nmol in 100 nL) injected into the NTS of rats increased arterial pressure from 111 +/- 4 to 126 +/- 5 mm Hg, and this effect was reversed by an ipsilateral microinjection of carbon monoxide into the NTS. Accordingly, the pressor effect of ZnDPBG may rely on inhibition of carbon monoxide production in the NTS. This implies that carbon monoxide formed by brain heme oxygenase plays a role in the central regulation of arterial pressure.

Animals↗

PubMed1997

Autonomic processing of the cardiovascular reflexes in the nucleus tractus solitarii.

The nucleus tractus solitarii (NTS) receives afferent projections from the arterial baroreceptors, carotid chemoreceptors and cardiopulmonary receptors and as a function of this information produces autonomic adjustments in order to maintain arterial blood pressure within a narrow range of variation. The activation of each of these cardiovascular afferents produces a specific autonomic response by the excitation of neuronal projections from the NTS to the ventrolateral areas of the medulla (nucleus ambiguous, caudal and rostal ventrolateral medulla). The neurotransmitters at the NTS level as well as the excitatory amino acid (EAA) receptors involved in the processing of the autonomic responses in the NTS, although extensively studied, remain to be completely elucidated. In the present review we discuss the role of the EAA L-glutamate and its different receptor subtypes in the processing of the cardiovascular reflexes in the NTS. The data presented in this review related to the neurotransmission in the NTS are based on experimental evidence obtained in our laboratory in unanesthetized rats. The two major conclusions of the present review are that a) the excitation of the cardiovagal component by cardiovascular reflex activation (chemo- and Bezold-Jarisch reflexes) or by L-glutamate microinjection into the NTS is mediated by N-methyl-D-aspartate (NMDA) receptors, and b) the sympatho-excitatory component of the chemoreflex and the pressor response to L-glutamate microinjected into the NTS are not affected by the NMDA receptors antagonist, suggesting that the sympatho-excitatory component of these responses is mediated by non-NMDA receptors.

Animals↗

PubMed1996

Commissural nucleus of the solitary tract lesions reduce food intake and body weight gain in rats.

This study investigated the effects of an electrolytic lesion of the commissural subnucleus of the nucleus of the solitary tract (commNTS) on body weight, daily food and water intake, and plasma glucose and insulin in rats. In the first 6 days following brain surgery, commNTS lesioned rats reduced daily food intake by 80% compared to rats with sham lesions. After this period rats with lesions of commNTS started recovering food intake, but intake remained significantly reduced until the 12th day after surgery. A reduction in body weight was observed 4 days after surgery and reached a maximum on the 12th day. After this, a partial recovery of body weight was observed, but weight remained significantly reduced compared to weights of rats with sham lesions through the conclusion of the study. Food intake and body weight gain in other rats with partial lesions of the commNTS or with lesions outside the commNTS did not differ from rats with sham lesions with regard to those variables. Daily water intake and plasma glucose and insulin were not changed by the commNTS lesions. These results suggest that commNTS is involved with mechanisms that control food intake and body weight in rats.

Animals↗

PubMed1996

Commissural NTS contributes to pressor responses to glutamate injected into the medial NTS of awake rats.

In the present study we investigated whether interruption of the chemoreceptor reflex by an electrolytic lesion of the commissural subnucleus of the nucleus tractus solitarii (commNTS) influenced pressor and bradycardic responses induced by microinjection of L-glutamate (L-Glu) into the medial NTS (mNTS) of conscious rats. Seven days after sham lesions, seven rats demonstrated significant pressor [change in mean arterial pressure (MAP) = +33 +/- 3 mmHg] and bradycardic [change in heart rate (HR) = -74 +/- 8 beats/min (bpm)] responses to chemoreceptor reflex activation by intravenous injection of KCN. Likewise, L-Glu (1 nmol in 100 nl) injected into the mNTS in sham rats induced pressor (+29 +/- 2 mmHg) and bradycardic responses (-90 +/- 8 bpm). However, in 11 rats with lesions in commNTS, pressor and bradycardic chemoreceptor reflex responses were abolished, and injection of L-Glu into the mNTS decreased MAP (-14 +/- 6 mmHg) and HR (-59 +/- 16 bpm) as is reported in anesthetized control rats. We conclude that pressor responses induced by L-Glu microinjected into the baroreceptor reflex region of mNTS in conscious rats depend on the integrity of the commNTS, which plays an important role in central chemoreceptor reflex pathways.

Animals↗