Spinal NMDA receptors mediate pressor responses evoked from the rostral ventrolateral medulla

Bazil, Michelle K.; Gordon, Frank J.

doi:10.1152/ajpheart.1991.260.1.h267

Cited by 29 publications

(12 citation statements)

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“…[21][22][23][24][25] It has also been suggested to be involved in the modulation of different cardiovascular reflexes, including baroreflexes and chemoreflexes. 26,27 In such situations, L-glutamate can be released or inhibited, depending on the quality of information and location of the response.…”

Section: Discussionmentioning

confidence: 99%

Nitric Oxide–Dependent Guanylyl Cyclase Participates in the Glutamatergic Neurotransmission Within the Rostral Ventrolateral Medulla of Awake Rats

1999

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Abstract-A well-known action of nitric oxide (NO) is to stimulate the soluble form of guanylyl cyclase, evoking an accumulation of cyclic GMP in target cells. The aim of the present study was to examine the effects of inhibition of guanylyl cyclase dependent on NO during cardiovascular responses induced by L-glutamate and S-nitrosoglutathione (SNOG) microinjected into the rostral ventrolateral medulla (RVLM) of awake rats. Three days before the experiments, adult male Wistar rats (280 to 320 g) were anesthetized for implantation of guide cannulas to the desired stereotaxic position (APϭϪ2.5 mm, Lϭ1.8 mm) in relation to lambda. The cannulas were fixed to the skull with acrylic cement. Twenty-four hours before the experiments, a femoral artery and vein were cannulated for recording arterial pressure (AP) and heart rate (HR) and injection of anesthetic. Unilateral microinjections (100 nL) of L-glutamate (5 nmol/L) and SNOG (2.5 nmol/L) were made into the histologically confirmed RVLM. The cardiovascular responses to these drugs were evaluated before and after microinjection (3 nmol/L, 200 nL) of either methylene blue or oxodiazoloquinoxaline (ODQ). The hypertensive effect of L-glutamate was attenuated by 74% after methylene blue (⌬APϭ49Ϯ8 to 13Ϯ4 mm Hg) and by 80.5% after ODQ (⌬APϭ30Ϯ2 to 6Ϯ2 mm Hg). The increase in AP produced by SNOG was fully blocked by ODQ (⌬APϭ39Ϯ8 to 1Ϯ2 mm Hg). These data indicate that cyclic GMP mechanisms have a key role in glutamatergic neurotransmission in the RVLM of awake rats, and it is most probable that NO participates in this response. Key Words: glutamic acid Ⅲ blood pressure, arterial Ⅲ brain Ⅲ nitric oxide Ⅲ rostral ventrolateral medulla Ⅲ guanylate cyclase I t is well known that sympathoexcitatory neurons of the rostral ventrolateral medulla (RVLM) directly innervate sympathetic preganglionic neurons in the intermediolateral cell columns of the spinal cord, which are involved in the regulation of vasomotor and cardiac tone. In its turn, the RVLM is highly connected to other areas of the central nervous system. In these vasomotor pathways, the major neurotransmitter used for fast synaptic transmission seems to be glutamate. In support of its importance in regulating blood pressure, glutamate microinjected into the RVLM produces an increase in arterial pressure (AP). 1 The concept that nitric oxide (NO) has a role, during stimulation of N-methyl-D-aspartate (NMDA) receptors, through activation of guanylyl cyclase (GC) is now well established. [2][3][4][5][6][7][8][9] The molecular mechanism of this NO-induced stimulation of cyclic GMP formation has been the subject of detailed investigations, and it has been suggested that NO interacts with the heme group bound to soluble GC in various tissues. 8,10 Although inhibitory effects evoked by NO have been described within the RVLM, 11-13 an opposite action, ie, excitatory effects, began to emerge in the literature, either in anesthetized as well as unanesthetized animals. 14,15 The microinjection of the nitrosothiols sodium nitroprussi...

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Section: Discussionmentioning

confidence: 99%

Nitric Oxide–Dependent Guanylyl Cyclase Participates in the Glutamatergic Neurotransmission Within the Rostral Ventrolateral Medulla of Awake Rats

1999

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“…The presence and participation of glutamate, an excitatory amino acid neurotransmitter, in cardiovascular centers have been extensively documented (41)(42)(43)(44)(45). This neurotransmitter seems to mediate and/or regulate functions during cardiovascular reflexes, including baroreflexes or chemoreflexes, and muscle pressor responses (41,(46)(47)(48)(49).…”

Section: Modulation By Brainstem Areasmentioning

confidence: 99%

Cardiovascular and autonomic modulation by the central nervous system after aerobic exercise training

Martins‐Pinge

2011

Braz J Med Biol Res

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The autonomic nervous system plays a key role in maintaining homeostasis under normal and pathological conditions. The sympathetic tone, particularly for the cardiovascular system, is generated by sympathetic discharges originating in specific areas of the brainstem. Aerobic exercise training promotes several cardiovascular adjustments that are influenced by the central areas involved in the output of the autonomic nervous system. In this review, we emphasize the studies that investigate aerobic exercise training protocols to identify the cardiovascular adaptations that may be the result of central nervous system plasticity due to chronic exercise. The focus of our study is on some groups of neurons involved in sympathetic regulation. They include the nucleus tractus solitarii, caudal ventrolateral medulla and the rostral ventrolateral medulla that maintain and regulate the cardiac and vascular autonomic tonus. We also discuss studies that demonstrate the involvement of supramedullary areas in exercise training modulation, with emphasis on the paraventricular nucleus of the hypothalamus, an important area of integration for autonomic and neuroendocrine responses. The results of these studies suggest that the beneficial effects of physical activity may be due, at least in part, to reductions in sympathetic nervous system activity. Conversely, with the recent association of physical inactivity with chronic disease, these data may also suggest that increases in sympathetic nervous system activity contribute to the increased incidence of cardiovascular diseases associated with a sedentary lifestyle.

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“…Multibarreled glass pipettes were placed into the RVLM, and microinjections were made using techniques described in detail previously. 29 - 30 Microinjections into the RVLM of various doses of L-glutamate (GLU) (0.05 to 10 nmol/50 nL) were made over a period of 5 to 15 seconds, and changes in mean arterial pressure (MAP) and heart rate were recorded. Each rat received in random order two to five doses of GLU with at least 5 minutes allowed between each injection.…”

Section: Stimulation Of the Rostral Ventrolateral Medullamentioning

confidence: 99%

Increased dietary salt sensitizes vasomotor neurons of the rostral ventrolateral medulla.

Pawloski-Dahm

Gordon

1993

Hypertension

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Excess dietary sodium is a major contributing factor to the incidence and severity of hypertension. However, the precise mechanism or mechanisms by which salt contributes to the severity of hypertension are unknown. The region of the rostral ventrolateral medulla (RVLM) is a principal brain stem locus critical for the regulation of arterial blood pressure by the sympathetic nervous system. The purpose of this study was to determine if excess dietary sodium chloride might alter the function or responsiveness of neurons In the RVLM. Male Sprague-Dawiey rats were given either tap water or 0.9% sodium chloride solution to drink for 10 to 14 days. Excess sodium chloride did not affect baseline blood pressure. However, when neurons of the RVLM were stimulated by microinjections of L-glutamate, evoked increases in arterial pressure were potentiated in rats given sodium chloride. Augmented pressor responses could not be accounted for by increased vascular reactivity because both groups responded similarly to intravenously administered phenylephrine and norepinephrine. Additionally, electrical stimulation of descending spinal sympathoexcitatory axons produced identical pressor responses in both groups, indicating that altered synaptic transmission at central or peripheral neuroeffector junctions distal to the RVLM could not explain enhanced pressor responses produced by direct stimulation of RVLM cell somata. Finally, impaired arterial baroreceptor reflexes could not account for augmented RVLM pressor responses, as depressor and bradycardic responses produced by electrical stimulation of aortic baroreceptor afferents were not reduced in rats given excess dietary sodium chloride. These results indicate that increased dietary salt intake sensitizes RVLM sympathoexcitatory neurons and may predispose toward the exaggerated expression of hypertension, suggesting a potential link between salt, hypertension, and the brain. (NaCl) to the pathogenesis of hypertension has been debated for almost half a century. 12 Although an increase in NaCl intake is not invariably associated with elevated arterial blood pressure, a large subset of individuals exhibits fluctuations in arterial pressure when daily salt intake is varied. 35 However, a diet high in salt alone is not sufficient to produce hypertension in otherwise normotensive individuals but instead plays a permissive role in enabling the exaggerated expression of hypertension.3 Salt sensitivity of blood pressure has been studied intensively, but the mechanism or mechanisms by which increased dietary salt imparts enhanced sensitivity to hypertensive stimuli are not known.In several experimental models of hypertension, excess NaCl intake is essential for either the development or full expression of hypertension.611 Additionally, the central nervous system (CNS) and peripheral sympathetic nervous system contribute significantly to the maintenance of elevated arterial pressure in many of

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Spinal NMDA receptors mediate pressor responses evoked from the rostral ventrolateral medulla

Cited by 29 publications

References 0 publications

Nitric Oxide–Dependent Guanylyl Cyclase Participates in the Glutamatergic Neurotransmission Within the Rostral Ventrolateral Medulla of Awake Rats

Nitric Oxide–Dependent Guanylyl Cyclase Participates in the Glutamatergic Neurotransmission Within the Rostral Ventrolateral Medulla of Awake Rats

Cardiovascular and autonomic modulation by the central nervous system after aerobic exercise training

Increased dietary salt sensitizes vasomotor neurons of the rostral ventrolateral medulla.

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