Navegando por Palavras-chave "sympathetic nerve activity"
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- ItemAcesso aberto (Open Access)Airway obstruction produces widespread sympathoexcitation: role of hypoxia, carotid chemoreceptors, and NTS neurotransmission(Wiley, 2018) Ferreira, Caroline B. [UNIFESP]; Cravo, Sergio L. [UNIFESP]; Stocker, Sean D.Obstructive sleep apnea (OSA) is the most common respiratory disturbance of sleep and is closely associated to cardiovascular diseases. In humans, apnea increases respiratory effort and elevates muscle sympathetic nerve activity (SNA), but the primary stimulus for the SNA activation has not been identified. We recently developed a model of apnea in rodents using acute airway obstruction. In this study, we employed this model to test whether the elevation in SNA was mediated by hypoxia, carotid chemoreceptors, or neurotransmission in the nucleus tractus solitarius (NTS). In anesthetized, male Sprague-Dawley rats, airway obstruction (20s) increased phrenic nerve activity (PNA), arterial blood pressure (ABP), and lumbar, renal, and splanchnic SNA. The changes in SNA were similar across all three sympathetic nerves. Inactivation of chemoreceptors by hyperoxia (100% O-2) or surgical denervation of carotid chemoreceptors attenuated, but did not eliminate, the changes in SNA and ABP produced by airway obstruction. To interrupt afferent information from carotid chemoreceptor and extracarotid afferents to the hindbrain, airway obstruction was performed before and after NTS microinjection of the GABA(A) agonist muscimol or a cocktail of NMDA and non-NMDA antagonists. Inhibition of NTS neurons or blockade of glutamatergic receptors attenuated the increase in lumbar SNA, splanchnic SNA, renal SNA, and PNA. Collectively, these findings suggest that PNA and SNA responses induced by airway obstruction depend, in part, on chemoreceptors afferents and glutamatergic neurotransmission in the NTS.
- ItemSomente MetadadadosChronic Antioxidant Treatment Improves Arterial Renovascular Hypertension and Oxidative Stress Markers in the Kidney in Wistar Rats(Nature Publishing Group, 2010-05-01) Nishi, Erika Emy [UNIFESP]; Oliveira-Sales, Elizabeth Barbosa [UNIFESP]; Bergamaschi, Cassia T. [UNIFESP]; Cesar Oliveira, Thais Galvao [UNIFESP]; Boim, Mirian A. [UNIFESP]; Campos, Ruy R. [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)BACKGROUNDSympathetic vasomotor hyperactivity and baroreflex dysfunction are involved in the development and maintenance of renovascular arterial hypertension. We hypothesized that angiotensin (Ang) II-dependent oxidative stress contributes to the pathophysiology of the two-kidney, one-clip (2K-1C) model.METHODSThe mean arterial pressure (MAP), baroreflex, and renal sympathetic nerve activity (rSNA) were evaluated after chronic administration of an antioxidant, vitamin C (vitC 150 mg/kg/day) in male Wistar 2K-1C rats. Additionally, the mRNA levels of Ang II subtype 1 receptor (AT(1)R), NAD(P)H oxidase subunits (p47phox and gp91phox), and major antioxidant enzymes were evaluated in the renal cortex.RESULTSAfter vitC treatment, the MAP (170 +/- 4 vs. 133 +/- 6 mm Hg; P < 0.05) and rSNA (161 +/- 5 vs. 118 +/- 12 spikes/s; P < 0.05) were significantly reduced only in the 2K-1C group. VitC improved the baroreflex control of heart rate (HR) and rSNA. the expression of AT(1)R, p47phox, and gp91phox was elevated (51, 184, and 132%, respectively) in the clipped kidney of 2K-1C group. VitC downregulated AT(1)R in the clipped kidney (31%). Catalase (CAT) expression was reduced in clipped (70%) and nonclipped (83%) kidneys of 2K-1C rats. VitC treatment augmented the expression of glutathione peroxidase (GPx) in both clipped (185%) and nonclipped (212%) kidneys of the 2K-1C group.CONCLUSIONSThe present study suggests a role for oxidative stress in the cardiovascular and sympathetic alterations in renovascular hypertension, associated with changes in the expression of AT,R, NAD(P)H oxidase subunits, and antioxidant enzymes in the kidney.
- ItemSomente MetadadadosDischarge of RVLM vasomotor neurons is not increased in anesthetized angiotensin II-salt hypertensive rats(Amer Physiological Soc, 2013-12-01) Pedrino, Gustavo R.; Calderon, Alfredo S.; Andrade, Mary Ann; Cravo, Sergio L. [UNIFESP]; Toney, Glenn M.; Universidade Federal de Goiás (UFG); Univ Texas Hlth Sci Ctr San Antonio; Universidade Federal de São Paulo (UNIFESP)Neurons of the rostral ventrolateral medulla (RVLM) are critical for generating and regulating sympathetic nerve activity (SNA). Systemic administration of ANG II combined with a high-salt diet induces hypertension that is postulated to involve elevated SNA. However, a functional role for RVLM vasomotor neurons in ANG II-salt hypertension has not been established. Here we tested the hypothesis that RVLM vasomotor neurons have exaggerated resting discharge in rats with ANG II-salt hypertension. Rats in the hypertensive (HT) group consumed a high-salt (2% NaCl) diet and received an infusion of ANG II (150 ng.kg(-1).min(-1) sc) for 14 days. Rats in the normotensive (NT) group consumed a normal salt (0.4% NaCl) diet and were infused with normal saline. Telemetric recordings in conscious rats revealed that mean arterial pressure (MAP) was significantly increased in HT compared with NT rats (P < 0.001). Under anesthesia (urethane/chloralose), MAP remained elevated in HT compared with NT rats (P < 0.01). Extracellular single unit recordings in HT (n = 28) and NT (n = 22) rats revealed that barosensitive RVLM neurons in both groups (HT, 23 cells; NT, 34 cells) had similar cardiac rhythmicity and resting discharge. However, a greater (P < 0.01) increase of MAP was needed to silence discharge of neurons in HT (17 cells, 44 +/- 5 mmHg) than in NT (28 cells, 29 +/- 3 mmHg) rats. Maximum firing rates during arterial baroreceptor unloading were similar across groups. We conclude that heightened resting discharge of sympathoexcitatory RVLM neurons is not required for maintenance of neurogenic ANG II-salt hypertension.
- ItemSomente MetadadadosInhibition of neurons in commissural nucleus of solitary tract reduces sympathetic nerve activity in SHR(Amer Physiological Soc, 2002-05-01) Sato, Monica A. [UNIFESP]; Colombari, Eduardo [UNIFESP]; Morrison, Shaun F.; Northwestern Univ; Universidade Federal de São Paulo (UNIFESP)Neurons in the commissural nucleus of the solitary tract (commNTS) play an important role in certain cardiovascular responses dependent on sympathetic vasoconstrictor activation, including the arterial chemoreceptor reflex. Electrolytic lesions of the commNTS elicit a fall in arterial pressure (AP) in spontaneously hypertensive rats (SHR). To determine whether the latter result 1) arose from elimination of commNTS neuronal activity rather than en passant axons and 2) was accompanied by a reduction in sympathetic nerve activity, we evaluated the effect of inhibition of neurons in the commNTS on basal splanchnic sympathetic nerve activity (SNA), AP, and heart rate (HR) in SHR, Wistar-Kyoto (WKY), and Sprague-Dawley (SD) rats. in chloralose-anesthetized, paralyzed, and artificially ventilated SHR, microinjection of GABA into the commNTS markedly decreased splanchnic SNA, AP, and HR. the reductions in SNA and AP following similar microinjections in WKY and SD rats were significantly less than those in SHR. Our findings suggest that tonically active neurons in the commNTS contribute to the maintenance of SNA and the hypertension in SHR. the level of tonic discharge of these commNTS neurons in normotensive WKY and SD rats may be lower than in SHR.
- ItemSomente MetadadadosMacrophage Migration Inhibitory Factor in the Paraventricular Nucleus Plays a Major Role in the Sympathoexcitatory Response to Salt(Lippincott Williams & Wilkins, 2010-11-01) Colombari, Eduardo [UNIFESP]; Colombari, Debora Simões de Almeida; Li, Hongwei; Shi, Peng; Dong, Ying; Jiang, Nan; Raizada, Mohan K.; Sumners, Colin; Murphy, David; Paton, Julian Francis Richmond; Univ Bristol; Univ Florida; São Paulo State Univ; Universidade Federal de São Paulo (UNIFESP)Central hyperosmotic stimulation (HS) evokes increases in sympathetic nerve activity mediated by activation of angiotensin type 1 receptors in the hypothalamic paraventricular nucleus (PVN). Macrophage inhibitory migration factor (MIF) is an intracellular inhibitory regulator of angiotensin type 1 receptor-mediated actions of angiotensin II within neurons of the PVN. MIF mediates its actions via its intrinsic thiol-protein oxidoreductase activity. We demonstrate that intracerebroventricular injection of hypertonic saline into Sprague-Dawley rats elicits a significant (approximate to 112%) increase in MIF mRNA expression in the PVN. Next, we evaluated the effect of viral-mediated expression of either MIF or [C60S]-MIF (which lacks thiol-protein oxidoreductase activity) in the PVN on the sympathoexcitation evoked by HS. We used a decorticate, arterially perfused in situ preparation of male Wistar rats (60 to 80 g). HS was induced by raising perfusate osmolality from 290 to 380 milliosmoles for 40 seconds. Seven to 10 days before experiments, rats were injected bilaterally (500 nL per side) with 0.9% saline (control) or with adenoassociated virus to express MIF, [C60S]-MIF, or enhanced green fluorescent protein in the PVN. HS produced sympathoexcitation in both the 0.9% saline and enhanced green fluorescent protein groups (sympathetic nerve activity increase of +27 +/- 4% and +25 +/- 4%, respectively; P<0.05), an effect that was not observed in the MIF group (+4 +/- 5%). Conversely, the HS-induced increase in sympathetic nerve activity was potentiated in the [C60S]-MIF group (+45 +/- 6%; P<0.05). We propose that MIF acting within the PVN is a major counterregulator of HS-induced sympathoexcitation, an effect that depends on thiol-protein oxidoreductase activity. (Hypertension. 2010;56:956-963.)
- ItemAcesso aberto (Open Access)Role of the medulla oblongata in normal and high arterial blood pressure regulation: the contribution of Escola Paulista de Medicina - UNIFESP(Academia Brasileira de Ciências, 2009-09-01) Cravo, Sergio Luiz [UNIFESP]; Campos, Ruy Ribeiro [UNIFESP]; Colombari, Eduardo [UNIFESP]; Sato, Mônica A.; Bergamaschi, Cassia Toledo [UNIFESP]; Pedrino, Gustavo Rodrigues [UNIFESP]; Ferreira-Neto, Marcos L.; Lopes, Oswaldo Ubriaco [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Faculdade de Medicina do ABC Departamento de Morfologia e Fisiologia; Federal de Uberlândia Faculdade de Educação FísicaSeveral forms of experimental evidence gathered in the last 37 years have unequivocally established that the medulla oblongata harbors the main neural circuits responsible for generating the vasomotor tone and regulating arterial blood pressure. Our current understanding of this circuitry derives mainly from the studies of Pedro Guertzenstein, a former student who became Professor of Physiology at UNIFESP later, and his colleagues. In this review, we have summarized the main findings as well as our collaboration to a further understanding of the ventrolateral medulla and the control of arterial blood pressure under normal and pathological conditions.