Relative effects of different spinal autonomic nuclei on cardiac sympathoexcitatory function (original) (raw)
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Brain Research, 1989
Sympathoexcitatory cardiovascular responses to the microinjections of L-glutamate into the intermediolateral cell column (IML) of the upper thoracic cord (C s to T4) were studied. Mean arterial pressure (MAP), heart rate (HR), the rate of increase in the left ventricular pressure (dP/dt) and contractility index were monitored in immobilized and artificially ventilated male Wistar rats anesthetized with pentobarbital or isofluorane. On the right side, microinjections (10-20 nl) of L-glutamate (0.9-1.77 nmol in 0.9% sodium chloride solution, pH 7.4) into the IML at T 2 level produced marked tachycardic responses with relatively small changes in contractility. On the left side, similar microinjections produced marked increase in dP/dt and contractility index with relatively small increase in HR.
Brain Research, 2006
Changes in heart rate (HR), thoracic sympathetic nerve activity (tSNA) and frequency of phrenic nerve discharge (PND) in response to microinjection of L-glutamate before and after local microinjection of ionotropic or metabotropic glutamate receptors antagonists into the commissural subnucleus of the NTS (comNTS) were investigated. The experiments were performed in an in situ unanesthetized decerebrated working heart-brainstem preparation (WHBP), and the main findings were as follows: (a) microinjection of increasing concentrations of L-glutamate (5, 25, 50, 250 and 500 mM) into the comNTS produced bradycardia, increase in tSNA and reduction in the frequency of the PND in a concentration-dependent manner; (b) both bradycardia and increase in tSNA were almost abolished by kynurenic acid (KYN, 250 mM, a nonselective ionotropic glutamate receptor antagonist); (c) the reduction in the frequency of the PND was reversed to an increase in the frequency of the PND after KYN and this increase was blocked by the sequential microinjection of MCPG (100 mM, a nonselective metabotropic glutamate receptor antagonist); and (d) microinjection of increasing concentrations of trans-ACPD (0.5, 1.0, 2.5, 5.0 and 10 mM, a metabotropic glutamate receptor agonist), elicited bradycardia and increase in the frequency of the PND in a concentration-dependent manner, which were blocked by MCPG. Taken together, these data indicate that L-glutamate and its ionotropic receptors are involved in the sympathoexcitatory, bradycardic and reduction in the frequency of the PND responses whereas/although its metabotropic receptors are involved in the bradycardic and mainly in the increase in the frequency of the PND to microinjection of L-glutamate into the comNTS in the WHBP.
Autonomic processing of the cardiovascular reflexes in the nucleus tractus solitarii
Brazilian Journal of Medical and Biological Research, 1997
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 ambiguus, caudal and rostral 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 an NMDA receptor antagonist, suggesting that the sympatho-excitatory component of these responses is mediated by non-NMDA receptors.
Brain Research, 1991
Microinlections of L-glutamate into the intermediolateral column of the spinal cord (IML) at T1-T 3 produced increases in heart rate (predominantly from the right IML) and myocardial contractility (predominantly from the left IML). Maximum responses were elicited from T 2 segment. At this site, microinjections of alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA), quisqualic acid, kainic add and N-methyl-D-aspartic acid (NMDA) produced dose-dependent increases in heart rate and contractility which were blocked by kynurenate (a non-selective excitatory amino acid receptor antagonist). D-2-Amlnophosphonoheptanoate (DAP-7) blocked the effects of NMDA but not kalnic acid, quisqualic acid and AMPA. Bilateral microinlections of kynurenate (2 nmol) and DAP-7 (5 nmol) into the IML at T1-T 3 significantly decreased the baseline values for contractility index and blocked the usual increase in contractility induced by unilateral microinlections of L-glutamate (1.77 nmol) into the ventrolateral medullary pressor area (VLPA). These observations suggest that: (1) a tome excitatory input, involving an NMDA-Iike amino acid as a transmitter, is present in the IML at T1-T 3 and (2) the stimulation of VLPA neurons results in the release of an NMDA-Iike excitatory amino acid in the IML at this level.
The Journal of physiology, 1987
1. In cats anaesthetized with chloralose, neuronal cell bodies were excited by micro-injection of DL-homocysteic acid (DLH). 2. Injections made into the ventrolateral medulla in the region of nucleus paragigantocellularis lateralis (p.g.l.) produced a rise in blood pressure accompanied by either an increase or decrease in heart rate according to the precise site of the injection. The tachycardia was blocked by propranolol (0.15-0.5 mg kg-1 I.V.) whilst bradycardia was abolished by vagotomy or atropine (0.2-1.5 mg kg-1 I.V.). 3. Recordings were made of blood flow to the hind-limb, renal and mesenteric vascular beds in order to study the haemodynamic changes separately in each region. 4. Vasoconstriction was seen in the renal and mesenteric beds and either vasodilatation or vasoconstriction could be evoked in hind-limb muscle. The vasodilatation in hind-limb muscle was resistant to atropine but significantly reduced by propranolol (0.15-1.5 mg kg-1 I.V.) and therefore was probably med...
The Journal of physiology, 2007
Peripheral chemoreflex activation with potassium cyanide (KCN) in awake rats or in the working heart-brainstem preparation (WHBP) produces: (a) a sympathoexcitatory/pressor response; (b) bradycardia; and (c) an increase in the frequency of breathing. Our main aim was to evaluate neurotransmitters involved in mediating the sympathoexcitatory component of the chemoreflex within the nucleus tractus solitarii (NTS). In previous studies in conscious rats, the reflex bradycardia, but not the pressor response, was reduced by antagonism of either ionotropic glutamate or purinergic P2 receptors within the NTS. In the present study we evaluated a possible dual role of both P2 and NMDA receptors in the NTS for processing the sympathoexcitatory component (pressor response) of the chemoreflex in awake rats as well as in the WHBP. Simultaneous blockade of ionotropic glutamate receptors and P2 receptors by sequential microinjections of kynurenic acid (KYN, 2 nmol (50 nl)(-1)) and pyridoxalphosphat...
Brain research, 2005
Our previous studies have demonstrated that stimulation of cardiac sympathetic afferents activates neurons in the parabrachial nucleus (PBN), a region known to play a role in central integration of cardiovascular autonomic reflexes. However, phenotypes of these activated neurons have not been well identified. Glutamate, an important excitatory neurotransmitter in the brain, is involved in PBN-mediated cardiovascular responses. Recent identification of vesicular glutamate transporter 3 (VGLUT3) has provided a novel and unique marker to locate distinctive perikarya of neurons that use glutamate as a neurotransmitter. The action of glutamate in the brain is influenced by nitric oxide. Thus, using triple immunofluorescent labeling, the present study examined expression of c-Fos, an immediate early gene, in the neurons containing VGLUT3 and neuronal nitric oxide synthase (nNOS) in the PBN following stimulation of cardiac sympathetic afferents. In anesthetized cats with bilateral barodenervation and cervical vagotomy, topical application of bradykinin (BK, 1-10 Ag/ml, 50 Al, n = 6) on the left ventricle was performed six times, every 20 min. Repeated administration of BK elicited consistent increases in blood pressure over a 100 min period while no changes were noted in the animals treated with the vehicle for BK (0.9% saline, n = 5). Compared to control cats, c-Fos expression was increased significantly in the cell bodies containing VGLUT3 as well as both VGLUT3 and nNOS in the external lateral PBN (elPBN) in BK-treated animals (all P < 0.01). In addition, using similar triple-staining method, we noted that fibers of activated neurons containing nNOS in the elPBN co-localized with vesicular glutamate transporter 2 following BK stimulation. These data suggest that glutamatergic neurons represent a cell type in the PBN that is activated by stimulation of cardiac sympathetic afferents. Nitric oxide has the potential to influence the action of glutamatergic neurons in regulation of excitatory cardiovascular responses induced by activation of cardiac sympathetic afferents.
Hypertension Research, 2000
The aim of the present study was to examine the effects of L-glutamate and glycine microinjected into the rostral ventrolateral medulla (RVLM) in conscious unrestrained rats. Microinjection of 2 nmol of L-glutamate increased the mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA) in the conscious rats. The RSNA responses were significantly larger in the conscious rats than in anesthetized rats, while the magnitude of the pressor responses was similar in conscious and urethane-anesthetized rats. L-Glutamate injection significantly decreased heart rate in the conscious rats, whereas it increased the heart rate slightly but not significantly in the anesthetized rats. Microinjection of 100 nmol of glycine into the RVLM of conscious rat decreased MAP and RSNA. In 2 of the 6 rats examined, the depressor and sympathoinhibitory responses were preceded by a few seconds of a pressor and sympathoexcitatory phase. The decreases of RSNA in response to glycine injection were significantly larger in the conscious rats than in the anesthetized rats, whereas the magnitude of the depressor responses was similar in the two groups of rats. Heart rate decreased in response to glycine injection into the RVLM in the conscious and the anesthetized rats. In conclusion, in conscious unrestrained rats, as well as in urethane-anesthetized rats, L-glutamate acts as a sympathoexcitatory agent and glycine acts as a sympathoinhibitory agent in the RVLM. The sympathetic responses to these amino acids are larger in conscious rats than in anesthetized rats.