Navegando por Palavras-chave "rostral ventrolateral medulla"

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    alpha(2)-adrenergic receptors are not required for central anti-hypertensive action of moxonidine in mice
    (Elsevier B.V., 2000-04-17) Tolentino-Silva, Fatima Rosaria Paulino [UNIFESP]; Haxhiu, M. A.; Waldbaum, S.; Dreshaj, I. A.; Ernsberger, P.; Case Western Reserve Univ; Universidade Federal de São Paulo (UNIFESP)
    In the mouse medulla oblongata, we characterized binding properties and functional responses of two recognition sites for imidazoline compounds: I-1-imidazoline and alpha(2)-adrenergic receptors. the mouse medulla expresses a higher density of I-1-receptors than in the rat, whereas alpha(2)-receptor densities were similar between the two species. in anesthetized, ventilated and paralyzed mice, we tested the hypotensive actions of the I-1/alpha(2) agonist moxonidine, determined its central site of its actions, and the relative roles of I-1 and alpha(2)-receptors. Experiments were performed in C(57)Bl(6) wild type and alpha(2A)-adrenergic receptor deficient mice. in both types of mice, neuronal activation within the rostral ventrolateral medulla (RVLM) region by glutamate microinjection elicited increases in arterial pressure. Moxonidine (0.5 nmol/site/10 nl) microinjected bilaterally into this vasopressor region decreased arterial pressure by 30% and heart rate by 11% in wild type mice. Efaroxan, the I-1/alpha(2) antagonist (0.4 nmol) when microinjected into the RVLM elevated blood pressure itself and abolished the action of moxonidine, whereas alpha(2)-blockade with SK&F 86466 had no significant effect on blood pressure and did not attenuate moxonidine's effect. To more definitively test the role of alpha(2)-adrenergic receptors in the action of moxonidine, moxonidine was microinjected into the RVLM of alpha(2A)-adrenergic deficient mice. the decreases in arterial pressure were nearly identical to those of wild type mice, whereas bradycardia was attenuated. Thus, in the mouse moxonidine acts within the RVLM region to lower arterial pressure mainly through the I-1-imidazoline receptor independent of alpha(2)-adrenergic receptors. (C) 2000 Published by Elsevier Science B.V. All rights reserved.
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    AV3V lesions reduce the pressor response to L-glutamate into the RVLM
    (Elsevier B.V., 2006-05-01) Vieira, A. A.; Colombari, E.; De Luca, L. A.; Colombari, DSD; Menani, J. V.; Paulista State Univ; Universidade Federal de São Paulo (UNIFESP)
    Neurons from the rostral ventrolateral medulla (RVLM) directly activate sympathetic preganglionic neurons in the spinal cord. Hypertensive responses and sympathetic activation produced by different stimuli are strongly affected by lesions of the preoptic periventricular tissue surrounding the anteroventral third ventricle (AV3V region). Therefore, in the present study, we investigated the effects of acute (1 day) and chronic (IS days) electrolytic lesions of the AV3V region on the pressor responses produced by injections of the excitatory amino acid L-glutamate into the RVLM of unanesthetized rats. Male Holtzman rats with sham or electrolytic AV3V lesions and a stainless steel cannula. implanted into the RVLM were used. the pressor responses produced by injections of L-glutamate (1, 5 and 10 nmol/100 nl) into the RVLM were reduced 1 day (9 +/- 4, 39 +/- 6 and 37 +/- 4 mm Hg, respectively) and 15 days after AV3V lesions (13 +/- 6, 39 +/- 4 and 43 +/- 4 mm Hg, respectively, vs. sham lesions: 29 +/- 3, 50 +/- 2 and 58 +/- 3 mm Hg, respectively). Injections of L-glutamate into the RVLM in sham or AV3V-lesioned rats produced no significant change in the heart rate (HR). Baroreflex bradycardia and tachycardia produced by iv phenylephrine or sodium nitroprusside, respectively, and the pressor and bradycardic responses to chemoreflex activation with iv potassium cyanide were not modified by AV3V lesions. the results suggest that signals from the AV3V region are important for sympathetic activation induced by L-glutamate into the RVLM. (c) 2006 Elsevier B.V. All rights reserved.
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    Central cholinergic blockade reduces the pressor response to L-glutamate into the rostral ventrolateral medullary pressor area
    (Elsevier B.V., 2007-06-25) Antonio Vieira, Alexandre; Colombari, Eduardo; De Luca, Laurival A.; Almeida Colombari, Debora Simoes de; Menani, Jose V.; UNESP; Universidade Federal de São Paulo (UNIFESP)
    Injections of the excitatory amino acid L-glutamate (L-glu) into the rostral ventrolateral medulla (RVLM) directly activate the sympathetic nervous system and increase mean arterial pressure (MAP). A previous study showed that lesions of the anteroventral third ventricle region in the forebrain reduced the pressor response to L-glu into the RVLM. in the present study we investigated the effects produced by injections of atropine (cholinergic antagonist) into the lateral ventricle (LV) on the pressor responses produced by L-ghl into the RVLM. Male Holtzman rats (280-320 g, n=5 to 12/group) with stainless steel cannulas implanted into the RVLM, LV or 4th ventricle (4th V) were used. MAP and heart rate (HR) were recorded in unanesthetized rats. After saline into the LV, injections of L-glu (5 nmol/100 nl) into the RVLM increased MAP (51 +/- 4 mm Hg) without changes in HR. Atropine (4 nmol/1 PI) injected into the LV reduced the pressor responses to L-glu into the RVLM (36 +/- 5 mm Hg), However, atropine at the same dose into the 4th V or directly into the RVLM did not modify the pressor responses to L-glu into the RVLM (45 +/- 2 and 49 +/- 4 mm Hg, respectively, vs. control: 50 +/- 4mmHg). Central cholinergic blockade did not affect baro and chemoreflex nor the basal MAP and HR. the results suggest that cholinergic mechanisms probably from forebrain facilitate or modulate the pressor responses to L-glu into the RVLM. the mechanism is activated by acetylcholine in the forebrain, however, the neurotransmitter released in the RVLM to facilitate the effects of glutamate is not acetylcholine. (C) 2007 Elsevier B.V. All rights reserved.
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    Differential baroreceptor modulation mediated by the ventrolateral medulla
    (Elsevier B.V., 2006-06-30) Bergamaschi, Cassia de Toledo; Carillo, Bruno de Arruda; Neto, Henrique Azevedo Futuro; Campos, Ruy Ribeiro de; Universidade Federal de São Paulo (UNIFESP); Univ Fed Espirito Santo; Escola Super Ciencias Santa Casa Misericordia Vit
    Previous studies have shown that pharmacological stimulation of a region denominated caudal pressor area (CPA), located in the caudal end of the ventrolateral medulla, induces increases in arterial blood pressure (BP). the aim of this study was to compare the responses on renal sympathetic nerve activity (rSNA) and BP responses mediated by stimulation of CPA or rostral ventrolateral medulla (RVLM), in intact or sino-aortic barodenervated rats. Male Wistar rats (300-350g, n = 15) were anesthetized (urethane 1.2 to 1.4g/kg, i.v.) and artificially ventilated. the mean arterial pressure (MAP) and rSNA were measured during bilateral glutamate microinjection (10nmo/100nl) into the CPA or into the RVLM. Glutamatergic stimulation of the RVLM increased MAP (46 +/- 7mm Hg) and rSNA (82 +/- 21%); during CPA stimulation, MAP and rSNA increased 60 +/- 7 mm Hg and 93 +/- 9%, respectively. However, despite the similarity of responses mediated by both regions, the duration of rSNA and blood pressure responses mediated by the CPA were significantly longer than the duration of the responses. mediated by the RVLM. After barodenervation, there was an increase in the time-course and magnitude of sympathetic response only in response to RVLM stimulation but not in response to CPA. the results suggest a differential baroreceptor modulation on rSNA mediated by the ventrolateral medulla neurons. Glutamatergic activation of CPA neurons can cause large increases in the rSNA and BP with a weaker baroreceptor modulation when compared to responses mediated by the RVLM neurons. (c) 2006 Elsevier B.V. All rights reserved.
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    Differential cardiorespiratory control elicited by activation of ventral medullary sites in mice
    (Amer Physiological Soc, 2000-08-01) Tolentino-Silva, Fatima Rosaria Paulino [UNIFESP]; Haxhiu, M. A.; Ernsberger, P.; Waldbaum, S.; Dreshaj, I. A.; Case Western Reserve Univ; Universidade Federal de São Paulo (UNIFESP)
    We studied the respiratory and blood pressure responses to chemical stimulation of two regions of the ventral brainstem in mice: the rostral and caudal ventrolateral medulla (RVLM and CVLM, respectively). Stimulation of the RVLM by microinjections of the excitatory amino acid L-glutamate induced increases in diaphragm activity and breathing frequency, elevation of blood pressure (BP), and a slight increase in heart rate (HR). However, activation of the CVLM induced a decrease in breathing frequency, mainly due to prolongation of expiratory time (TE), and hypotension associated with a slight slowing of HR. Because adrenergic mechanisms are known to participate in the control of respiratory timing, we examined the role of alpha(2)-adrenergic receptors in the RVLM region in mediating these inhibitory effects. The findings demonstrated that blockade of the alpha(2)-adrenergic receptors within the RVLM by prior microinjection of SKF-86466 (an alpha(2)-adrenergic receptor blocker) significantly reduced changes in TE induced by CVLM stimulation but had little effect on BP responses. These results indicate that, in mice, activation of the RVLM increases respiratory drive associated with an elevation of BP, but stimulation of CVLM induces prolongation of TE via an alpha(2)-adrenergic signal transduction pathway.
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    Excitatory effects of nitric oxide within the rostral ventrolateral medulla of freely moving rats
    (Amer Heart Assoc, 1997-09-01) Pinge, Marli Cardoso Martins [UNIFESP]; Passy, Izabel Baraldi [UNIFESP]; Lopes, Oswaldo Ubriaco [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    The aim of the present study was to examine the participation of NO in the rostral ventrolateral medulla (RVLM) of freely moving rats. We utilized NO donors and L-arginine, which were microinjected into the RVLM. Unilateral microinjection (100 nL) of 2.5 nmol sodium nitroprusside produced a biphasic response consisting of an initial, rapid increase in arterial pressure (AP) from 125+/-5 to 161+/-8 mm Hg (P<.01) and a second, long-lasting response with a progressive increase in AP (maximum Delta peak, 34+/-9 mm Hg; P<.01). Another NO donor, S-nitroso-N-acetylpenicillamine (SNAP; 2.5 nmol), also produced immediate hypertension from 118+/-5 mm Hg to 168+/-7 mm Hg (P<.01) but without the second, long-lasting response. L-Arginine (5, 24, and 140 nmol) produced a gradual increase in AP. L-Glutamate (5 nmol) microinjected into the RVLM produced an increase in AP from 122+/-9 mm Hg to 171+/-8 mm Hg (P<.01) and bradycardia from 342+/-10 to 315+/-8 beats/min. This AP response was significantly attenuated, from 115+/-7 to 128+/-9 mm Hg (P<.05), after microinjection of methylene blue (3 nmol) without alterations In heart rate. These results indicate that NO may have an excitatory effect on the RVLM of freely moving rats, probably in association with glutamatergic synapses via cGMP mechanisms.
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    Glutamatergic and GABAergic inputs to the RVL mediate cardiovascular adjustments to noxious stimulation
    (Amer Physiological Soc, 2001-02-01) Possas, Olga Sueli [UNIFESP]; Lopes, Oswaldo Ubriaco [UNIFESP]; Cravo, Sergio Luiz [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Stimulation of cutaneous and muscle afferents induces several cardiovascular adjustments such as hypertension, tachycardia, and muscle vasodilation. Although previous studies have demonstrated that the rostral ventrolateral medulla (RVL) mediates sympathoexcitation and pressor responses to sciatic nerve stimulation (SNS), whether it also mediates blood flow adjustments remains unclear. Therefore, in the present study, we examined the role of the RVL in the vasodilation induced by SNS and the possible neurotransmitters involved. In Urethane-anesthetized, paralyzed, and artificially ventilated rats, SNS (square pulses, 1 ms, 20 Hz, 800-1200 muA, 10 s) produced increases in blood pressure, heart rate, blood flow, and vascular conductance of the stimulated limb. Unilateral microinjection of kainic acid (2 nmol/100 nl) into the RVL contralateral to the stimulated limb abolished cardiovascular adjustments to SNS. Unilateral microinjections of kynurenic acid (2 nmol/100 nl) selectively abolished the pressor response to SNS, whereas bicuculline (400 pmol/100 nl) abolished the increases in blood flow without changing the pressor response. These results suggest that glutamatergic synapses within the RVL mediate pressor responses, whereas GABAergic synapses may mediate the vasodilation to SNS.
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    Nitric oxide-dependent guanylyl cyclase participates in the glutamatergic neurotransmission within the rostral ventrolateral medulla of awake rats
    (Lippincott Williams & Wilkins, 1999-10-01) Pinge, Marli Cardoso Martins [UNIFESP]; Araujo, G. C.; Lopes, Oswaldo Ubriaco [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    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 (AP=-2.5 mm, L=1.8 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 (Delta A=49+/-8 to 13+/-4 mm Hg) and by 80.5% after ODQ (Delta AP=30+/-2 to 6+/-2 mm HS) The increase in AP produced by SNOG was fully blocked by ODQ (Delta AP=39+/-8 to 1+/-2 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.
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    The role of oxidative stress in renovascular hypertension
    (Wiley-Blackwell, 2011-02-01) Campos, Ruy R. [UNIFESP]; Oliveira-Sales, Elizabeth B. [UNIFESP]; Nishi, Erika E. [UNIFESP]; Boim, Mirian A. [UNIFESP]; Dolnikoff, Miriam S. [UNIFESP]; Bergamaschi, Cassia T. [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    P>1. There is mounting evidence that increased oxidative stress and sympathetic nerve activity play important roles in renovascular hypertension. in the present review, we focus on the importance of oxidative stress in two distinct populations of neurons involved with cardiovascular regulation: those of the rostral ventrolateral medulla (RVLM) and those of the paraventricular nucleus of the hypothalamus (PVN) in the maintenance of sympathoexcitation and hypertension in two kidney-one clip (2K1C) hypertensive rats. Furthermore, the role of oxidative stress in the clipped kidney is also discussed.2. in the studies reviewed in this article, it was found that hypertension and renal sympathoexcitation in 2K1C rats were associated with an increase in Angiotensin II type one receptor (AT(1)) expression and in oxidative markers within the RVLM, PVN and in the clipped kidneys of 2K1C rats. Furthermore, acute or chronic anti-oxidant treatment decreased blood pressure and sympathetic activity, and improved the baroreflex control of heart rate and renal sympathetic nerve activity in 2K1C rats. Tempol or vitamin C administration in the RVLM, PVN or systemically all reduced blood pressure and renal sympathetic activity. Cardiovascular improvement in response to chronic anti-oxidant treatment was associated with a downregulation of AT(1) receptors, as well as oxidative markers in the central nuclei and clipped kidney.3. the data discussed in the present review support the idea that an increase in oxidative stress within the RVLM, PVN and in the ischaemic kidney plays a major role in the maintenance of sympathoexcitation and hypertension in 2K1C rats.
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    Rostral ventrolateral medulla - A source of sympathetic activation in rats subjected to long-term treatment with L-NAME
    (Lippincott Williams & Wilkins, 1999-10-01) Bergamaschi, Cassia Toledo [UNIFESP]; Campos, Ruy Ribeiro [UNIFESP]; Lopes, Oswaldo Ubriaco [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    The major aim of the present study was to evaluate the role of the rostral ventrolateral medulla (RVLM) in the maintenance of hypertension in rats subjected to long-term treatment with N-G-nitro-L-arginine methyl ester (L-NAME) (70 mg/kg orally for 1 week). We inhibited or stimulated RVLM neurons with the use of drugs such as glycine, L-glutamate, or kynurenic acid in urethane-anesthetized rats (1.2 to 1.4 g/kg: IV). Bilateral microinjection of glycine (50 nmol. 100 nL) into the RVLM of hypertensive rats produced a decrease in mean arterial blood pressure (MAP) from 158+/-4 to 71+/-4 mm Hg (P<0.05), which was similar to the decrease produced by intravenous administration of hexamethonium. In normotensive rats, glycine microinjection reduced MAP from 106+/-4 to 60+/-3 mm Hg (P<0.05). Glutamate microinjection into the RVLM produced a significant increase in MAP in both hypertensive rats (from 157+/-3 to 201+/-6 mm Hg) and normotensive rats (from 105+/-5 to 148+/-9 mm Hg). No change in MAP was observed in response to kynurenic acid microinjection into the RVLM in either group. These results suggest that hypertension in response to long-term L-NAME treatment is dependent on an increase in central sympathetic drive, mediated by RVLM neurons. However, glutamatergic synapses within RVLM are probably not involved in this response.
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    Rostral ventrolateral medulla: An integrative site for muscle vasodilation during defense-alerting reactions
    (Kluwer Academic/plenum Publ, 2003-10-01) Cravo, S. L.; Possas, O. S.; Ferreira-Neto, M. L.; Universidade Federal de São Paulo (UNIFESP)
    1. Evidence gathered over the last 30 years has firmly established that the rostral ventrolateral medulla (RVLM) is a major vasomotor center in the brainstem, harboring sympathetic premotor neurons responsible for generating and maintaining basal vasomotor tone and resting levels of arterial blood pressure. Although the RVLM has been almost exclusively classified as a vasopressor area, in this report we review some evidence suggesting a prominent role of the RVLM in muscle vasodilation during defense-alerting responses.2. Defense-alerting reactions are a broad class of behavior including flexion of a limb, fight/flight responses, apologies, etc. They comprise species-distinctive motor and neurovegetative adjustments. Cardiovascular responses include hypertension, tachycardia, visceral vasoconstriction, and muscle vasodilation. Since defense-alerting reactions generally involve intense motor activation, muscle vasodilation is regarded as a key feature of these responses.3. in anesthetized or unanesthetized-decerebrate animals, natural or electrical stimulation of cutaneous and muscle afferents produced hypertension, tachycardia, and vasodilation restricted to the stimulated limb.4. Unilateral inactivation of the RVLM contralateral to the stimulated limb abolished cardiovascular adjustments to stimulation of cutaneous and muscle afferents. Within the RVLM glutamatergic synapses mediate pressor responses, whereas GABAergic synapses mediates muscle vasodilation.5. in urethane-anesthetized rats, electrical stimulation of the hypothalamus elicited hypertension, tachycardia, visceral vasoconstriction, and hindlimb vasodilation. the hindlimb vasodilation induced by hypothalamic stimulation is a complex response, involving reduction of sympathetic vasoconstrictor tone, release of catecholamines by the adrenal medulla, and a still unknown system that may use nitric oxide as a mediator.6. Blockade of glutamatergic transmission within the RVLM selectively blocks muscle vasodilation induced by hypothalamic stimulation.7. the results obtained suggest that, besides its role in the generation and maintenance of the sympathetic vasoconstrictor drive, the RVLM is also critical for vasodilatory responses during defense reactions. the RVLM may contain several, distinctive mechanisms for muscle vasodilation. Anatomical and functional characterization of these pathways may represent a breakthrough in our understanding of cardiovascular control in normal and/or pathological conditions.