Post-partum depression (PPD) with varying clinical manifestations affecting new parents remains underdiagnosed and poorly treated. This minireview revisits the pharmacotherapy, and relevant etiological basis, capable of advancing preclinical research frameworks. Maternal tasks accompanied by numerous behavioral readouts demand modeling different paradigms that reflect the complex and heterogenous nature of PPD. Hence, effective PPD-like characterization in animals towards the discovery of pharmacological intervention demands research that deepens our understanding of the roles of hormonal and non-hormonal components and mediators of this psychiatric disorder.

Aims: To determine the chronically effects of internal desynchrony on heart tissue, and on cardiac responses to ischemia-reperfusion (IR) in male rats.Methods: The animals were randomized into two groups: control (CTR) maintained under LD cycle of 12h:12h or desynchronized (DSC) under a symmetrical LD cycle of 11h:11h throughout eight weeks. The echocardiogram, Western Blotting, biochemical tests, and morphological analysis were performed on all animals. For DSC rats, their isolated hearts were perfused with Langendorff setup at different phase of locomotor activity, and cardiac responses after IR were measured.Key findings: In the DSC group mean of cardiomyocyte diameter was lower than in the CTR group, while the collagen content in the left ventricle increased. Furthermore, the catalase expression (CAT) as well as its activity in DSC hearts were increase compared with CTR. We also found that lipid peroxidation measurement (LPO) and quantification of carbonylated protein were increase in the DSC rat’s hearts. Ex vivo cardiac function was assessed at phase of coincidence or non-coincidence of locomotor activity from desynchronized rats. After ischemia, we observed that at non-coincidence phase the hearts showed higher values on perfusion pressure, left ventricular systolic and diastolic pressure than at coincidence phase.Significances: The results above suggest that the isolated heart of animals with circadian disruption of locomotor activity rhythm respond differently, according to time of day that ischemia was performed. Moreover, chronically internal circadian desynchronization increases oxidative stress led to an impairing remodeling of heart tissues.

Tapinanthus globiferus is often referred to as an all-purpose herb for the treatment of stroke and epilepsy. The present study investigates the anticonvulsant effect of methanolic leaf extract, active fractions, and lupeol (isolate) of Tapinanthus globiferus in mice as well as the underlying mechanisms. Following phytochemical studies of T. globiferus, preliminary assays were performed to evaluate MLE-induced toxic effect and behavioral changes. The pentylenetetrazol (70 mg/kg, i. p.)-induced seizure was evaluated in mice that were pretreated orally with vehicle 10 mL/kg, MLE (4, 20, or 100 mg/kg), fractions (F1 to F6), lupeol 10 mg/kg or diazepam (3 mg/kg). Methanolic leaf extract preserved neuron viability as well as the relative organ weight, and hematological and biochemical parameters. The behavioral endpoints, neuromuscular coordination, and sensory response parameters revealed a dose-dependent effect of methanolic leaf extract. This extract, active fractions, lupeol, and diazepam potentiated the hypno-sedative effect of the barbiturate and attenuated PTZ-induced acute seizure. This antiseizure effect was completely reversed by flumazenil 2 mg/kg (benzodiazepine site antagonist). Altogether, the benzodiazepine site-mediated anticonvulsant effects of methanolic leaf extract, active fractions, and lupeol corroborate traditional application of T. globiferus against epilepsy.

Disruptions in circadian rhythms have been associated with several diseases, including cardiovascular and metabolic disorders. Forced internal desynchronization induced by a period of T-cycles of 22 h (T22 protocol) reaches the lower limit of entrainment and dissociates the circadian rhythmicity of the locomotor activity into two components, driven by different outputs from the suprachiasmatic nucleus (SCN). The main goal of this study was to evaluate the cardiovascular and metabolic response in rats submitted to internal desynchronization by T22 protocol. Male Wistar rats were assigned to either a control group subjected to a usual T-cycles of 24 h (12 h-12 h) or an experimental group subjected to the T22 protocol involving a 22-h symmetric light-dark cycle (11 h-11 h). After 8 weeks, rats subjected to the T22 exhibited desynchrony in their locomotor activity. Although plasma glucose and insulin levels were similar in both groups, desynchronized rats demonstrated dyslipidemia, significant hypertrophy of the fasciculate zone of the adrenal gland, low IRB, IRS2, PI3K, AKT, SOD and CAT protein expression and an increased expression of phosphoenolpyruvate carboxykinase in the liver. Furthermore, though they maintained normal baseline heart rates and mean arterial pressure levels, they also presented reduced baroreflex sensitivity. The findings indicate that circadian timing desynchrony following the T22 protocol can induce cardiometabolic disruptions. Early hepatic metabolism dysfunction can trigger other disorders, though additional studies are needed to clarify the causes.

The infusion of hypertonic saline solution (HSS) is known to be beneficial to the treatment of hypovolemic hemorrhage (HH). The central mechanism of HSS-induced cardiovascular and autonomic recovery of animals subjected to HH remains unclear. Hence, the present study evaluated the involvement of median preoptic nucleus (MnPO) and medullary noradrenergic neurons (A1 and A2) in HSS-induced cardiovascular and sympathetic responses in hemorrhagic rats. The wistar rats were subjected to specific lesion of noradrenergic neurons through the nanoinjections of anti-DβH-saporin into caudal ventrolateral medulla (A1 neurons) and nucleus of the solitary tract (A2 neurons). After recovery, mean arterial pressure (MAP) and renal sympathetic nervous activity were recorded. The HH was performed through blood withdrawal until a MAP of 60 mmHg was attained. In sham rats, HSS infusion (3M NaCl) reestablished MAP without change in HH-induced sympathoinhibition. The muscimol (agonist of GABAA receptor) was nanoinjected in MnPO during HH and MnPO inhibition abolished the recovery of MAP and HSS-induced sympathoinhibition. Simultaneous lesions of A1 and A2 abolished MAP restoration and sympathoinhibition after HSS infusion. These results suggest that the recovery of MAP and HSS-induced sympathoinhibition in hemorrhaged rats depend on intact neural projections from A1 and A2 to MnPO.

IIntrathecal injection of bombesin (BBS) promoted hypertensive and sympathoexcitatory effects in normotensive (NT) rats. However, the involvement of rostral ventrolateral medulla (RVLM) in these responses is still unclear. In the present study, we investigated: (1) the effects of BBS injected bilaterally into RVLM on cardiorespiratory and sympathetic activity in NT and spontaneously hypertensive rats (SHR); (2) the contribution of RVLM bombesin type 1 receptors (BB1) to the maintenance of hypertension in SHR. Urethane-anesthetized rats (1.2 g · kg−1, i.v.) were instrumented to record mean arterial pressure (MAP), diaphragm (DIA) motor and renal sympathetic nerve activity (RSNA). In NT rats and SHR, BBS (0.3 mM) nanoinjected into RVLM increased MAP (33.9 ± 6.6 mmHg and 37.1 ± 4.5 mmHg, respectively; p < 0.05) and RSNA (97.8 ± 12.9 % and 84.5 ± 18.1 %, respectively; p < 0.05). In SHR, BBS also increased DIA burst amplitude (115.3 ± 22.7 %; p < 0.05). BB1 receptors antagonist (BIM-23127; 3 mM) reduced MAP (-19.9 ± 4.4 mmHg; p < 0.05) and RSNA (-17.7 ± 3.8 %; p < 0.05) in SHR, but not in NT rats (-2.5 ± 2.8 mmHg; -2.7 ± 5.6 %, respectively). These results show that BBS can evoke sympathoexcitatory and pressor responses by activating RVLM BB1 receptors. This pathway might be involved in the maintenance of high levels of arterial blood pressure in SHR.

The present study sought to determine the involvement of median preoptic nucleus (MnPO) in the regulation of the cardiovascular function and renal sympathetic activity in normotensive (NT) and spontaneously hypertensive rats (SHR). MnPO inhibition evoked by Muscimol (4mM) nanoinjections, elicited fall in MAP and renal sympathoinhibition in NT-rats. Surprisingly, in SHRs these responses were greater than in NT-rats. These results demonstrated, for the first time that MnPO was involved in the tonic control of sympathetic activity in NT and SHRs. Furthermore, our data suggest the MnPO involvement in the increased sympathetic outflow and consequent arterial hypertension observed in SHRs.

Hypernatremia stimulates the secretion of oxytocin (OT), but the physiological role of OT remains unclear. The present study sought to determine the involvement of OT and renal nerves in the renal responses to an intravenous infusion of hypertonic saline. Male Wistar rats (280-350 g) were anesthetized with sodium thiopental (40 mg. kg(-1), i.v.). A bladder cannula was implanted for collection of urine. Animals were also instrumented for measurement of mean arterial pressure (MAP) and renal blood flow (RBF). Renal vascular conductance (RVC) was calculated as the ratio of RBF by MAP. In anesthetized rats (n = 6), OT infusion (0.03 µg • kg(-1), i.v.) induced renal vasodilation. Consistent with this result, ex vivo experiments demonstrated that OT caused renal artery relaxation. Blockade of OT receptors (OXTR) reduced these responses to OT, indicating a direct effect of this peptide on OXTR on this artery. Hypertonic saline (3 M NaCl, 1.8 ml • kg(-1) b.wt., i.v.) was infused over 60 s. In sham rats (n = 6), hypertonic saline induced renal vasodilation. The OXTR antagonist (AT; atosiban, 40 µg • kg(-1) • h(-1), i.v.; n = 7) and renal denervation (RX) reduced the renal vasodilation induced by hypernatremia. The combination of atosiban and renal denervation (RX+AT; n = 7) completely abolished the renal vasodilation induced by sodium overload. Intact rats excreted 51% of the injected sodium within 90 min. Natriuresis was slightly blunted by atosiban and renal denervation (42% and 39% of load, respectively), whereas atosiban with renal denervation reduced sodium excretion to 16% of the load. These results suggest that OT and renal nerves are involved in renal vasodilation and natriuresis induced by acute plasma hypernatremia.

Changes in plasma osmolarity, through central and peripheral osmoreceptors, activate the median preoptic nucleus (MnPO) that modulates autonomic and neuroendocrine adjustments. The present study sought to determine the participation of MnPO in the cardiovascular recovery induced by hypertonic saline infusion (HSI) in rats submitted to hemorrhagic shock. The recordings of mean arterial pressure (MAP) and renal vascular conductance (RVC) were carried out on male Wistar rats (250–300 g). Hemorrhagic shock was induced by blood withdrawal over 20 min until the MAP values of approximately 60 mmHg were attained. The nanoinjection (100 nL) ofGABAAagonist (Muscimol 4 mM; experimental group (EXP)) or isotonic saline (NaCl 150 mM; control (CONT)) into MnPO was performed 2 min prior to intravenous overload of sodium through HSI (3 M NaCl, 1.8 mL/kg, b.wt.). Hemorrhagic shock reduced the MAP in control (62±1.1 mmHg) and EXP (61±0.4 mmHg) equipotently. The inhibition of MnPO impaired MAP (CONT:104±4.2versus EXP:60±6.2 mmHg) and RVC (CONT:6.4±11.4versus EXP:-53.5±10.0) recovery 10 min after HSI. The overall results in this study demonstrated, for the first time, that the MnPO plays an essential role in the HSI induced resuscitation during hypovolemic hemorrhagic shock.

Noradrenergic neurons in the caudal ventrolateral medulla (CVLM; A1 group) contribute to cardiovascular regulation. The present study assessed whether specific lesions in the A1 group altered the cardiovascular responses that were evoked by hypertonic saline (HS) infusion in non-anesthetized rats. Male Wistar rats (280-340 g) received nanoinjections of antidopamine-beta-hydroxylase-saporin (A1 lesion, 0.105 ng.nL(-1)) or free saporin (sham, 0.021 ng.nL(-1)) into their CVLMs. Two weeks later, the rats were anesthetized (2% halothane in O-2) and their femoral artery and vein were catheterized and led to exit subcutaneously between the scapulae. On the following day, the animals were submitted to HS infusion (3 M NaCl, 1.8 ml . kg(-1), b.wt., for longer than 1 min). In the sham-group (n = 8), HS induced a sustained pressor response (Delta MAP: 35 +/- 3.6 and 11 +/- 1.8 mmHg, for 10 and 90 min after HS infusion, respectively; P<0.05 vs. baseline). Ten min after HS infusion, the pressor responses of the anti-D beta H-saporin-treated rats (n = 11) were significantly smaller(Delta MAP: 18 +/- 1.4 mmHg; P<0.05 vs. baseline and vs. sham group), and at 90 min, their blood pressures reached baseline values (2 +/- 1.6 mmHg). Compared to the sham group, the natriuresis that was induced by HS was reduced in the lesioned group 60 min after the challenge (19 +/- 65.5 mM vs. 262 +/- 7.6 mM, respectively; P<0.05). In addition, A1-lesioned rats excreted only 47% of their sodium 90 min after HS infusion, while sham animals excreted 80% of their sodium. Immunohistochemical analysis confirmed a substantial destruction of the A1 cell group in the CVLM of rats that had been nanoinjected withanti-D beta H-saporin. These results suggest that medullary noradrenergic A1 neurons are involved in the excitatory neural pathway that regulates hypertensive and natriuretic responses to acute changes in the composition of body fluid.

Maintaining the composition and volume of the extracellular fluid (ECF) and intracellular fluid (ICF) within a restricted range of variation is critical for normal tissue perfusion and cellular function (Strange 1993). The ECF is primarily composed by the vascular and extravascular (interstitial) fluid, and has sodium as a determinant ion of its osmolarity and volume. The ECF/plasma volume ratio is of utmost importance for maintaining vascular capacitance and, consequently, venous return, cardiac output, and arterial pressure (Ramsay 1991). Maintaining the variability of the ECF volume within a strict range is a central goal of homeostatic mechanisms.The central nervous system (CNS) is informed about alterations in volume and tonicity of the ECF through the activity of peripheral and central sensory receptors. Receptors that respond to alterations in the volume of ECF are sensitive to the degree of mechanical distension of blood vessels or cardiac chamber (reviewed by Bourque 2008). They are located in the wall of the atrium and pulmonary vessels (cardiopulmonary receptors), and in the adventitia of the aortic arch/carotid sinus (arterial baroreceptors), or renal afferent arterioles (renal baroreceptors). These receptors mediate central autonomic reflexes through primary connections to the nucleus of the solitary tract (NTS) or mediate renorenal reflexes. Receptors that respond to alterations in ICF are sensitive to ECF tonicity or effective osmotic concentration (Bourque 2008; Kuramochi and Kobayashi 2000; McKinley et al. 1992). They are located in renal, intestinal, and hepatic vessels, in the wall of the gastrointestinal tract and oropharyngeal cavity and in brain circumventricular organs, notably area postrema, subfornical organ (SFO), and organum vasculosum of the lamina terminalis (OVLT). Efferent responses to the activation of these receptors include renal sympathetic nerve activity, hormone secretion [atrial natriuretic peptide (ANP), oxytocin, vasopressin, renin–angiotensin II], and hemodynamic changes. Such responses culminate in controlled alterations of renal sodium and water excretion.Among these several mechanisms and responses, we would like to call attention to those associated with ECF volume expansion. Dehydration is a menace to immediate survival, but volume expansion is associated with long-term changes that affect health, particularly hypertension and heart failure (reviewed by Antunes-Rodrigues et al. 2004; Toney and Stocker 2010; Toney et al. 2010). Conversely, hypertonic NaCl also has a potential therapeutic value to recovery from hemorrhagic shock (Pedrino et al. 2011; Rocha e Silva et al. 1986; Velasco et al. 1980). In this chapter, we will focus on cardiovascular responses to volume expansion and hypertonicity, their sensory afferences, and how these responses are subserved by a brainstem–hypothalamic–preoptic axis and its associated cathecolaminergic pathways.

O presente estudo buscou descrever a prevalencia da Dependencia de Exercicios Secundario (DESc, ou seja, atitudes alimentares de risco associadas com sintomas de dependencia de exercicios) entre homens e mulheres em uma populacao nao-atleta. Neste trabalho, 174 praticantes regulares de exercicios fisicos, entre 18 e 62 anos, quando abor- dados responderam a Escala de Dependencia de Exercicios (EDE) e ao Eating Attitudes Test (EAT-26). Houve mais mulheres do que homens com DESc. Contudo, somente os homens apresentaram sintomas de dependencia de exercicios com ausencia de atitudes alimentares de risco. Os transtornos alimentares podem ou nao ocorrer entre nao-atletas dependentes de exercicios fisicos, embora haja uma maior prevalencia de DESc entre as mulheres.

The present study sought to describe the prevalence of Secondary Exercise Dependence (ScED, i.e. eating disorders attitudes along with exercise dependence symptoms) may differ between men and women in a broader exercising population. In this study, 174 regularly exerciser, aged 18-62 years old, who were invited to respond the Exercise Dependence Scale (EDS) and the Eating Attitudes Test (EAT-26). There were more women than men with ScED. However, only men in the sample presented exercise dependence symptoms without eating disorders attitudes. Eating disorders may or may not exist in those who are exercise dependent in the broad exercising population, although there is a higher prevalence of ScED in women than men.

Studies have been shown that Median Preoptic Nucleus (MnPO) neurons have a great influence in the cardiovascular responses induced by changes in circulating volume. The present study sought to determine the participation of MnPO in the cardiovascular control. Male Wistar normotensive (NT) and spontaneously hypertensive (SH) rats (280–320g) were anesthetized with urethane (1.2 g/kg, i.v.) and instrumented for mean arterial blood pressure (MAP) and renal blood flow (RBF) recordings. Renal vascular conductance (RVC) was calculated as the ratio RBF/MAP and expressed as percentage of baseline. In NT rats (n=7), inhibition of MnPO nucleus produced a significant hypotension (−7 ± 1.5 mmHg) and renal vasodilation (5.3 ± 1.2% above baseline). In SH rats (n=8), hypotension response was significantly greater (−15 ± 2.7 mmHg, p<0.05) than NT rats. We also observed an increase of RVC (8.4 ± 2.4% above baseline) in HT rats. Analysis of the spread of dye nanoinjected at the end of the experiment showed that the drug injection sites were confined to the MnPO. We conclude that the MnPO nucleus is involved in the tonic regulation of blood pressure in NT rats. Moreover, the increase of neuronal activity in the MnPO may contribute to sympathoexcitation and maintenance of hypertension in SH rats. Supported by CNPq (477832/2010‐5; GRP).

Renal vasodilation and sympathoinhibition are recognized responses induced by hypernatremia, but the central neural pathways underlying such responses are not yet entirely understood. Several findings suggest that A2 noradrenergic neurons, which are found in the nucleus of the solitary tract (NTS), play a role in the pathways that contribute to body fluid homeostasis and cardiovascular regulation. The purpose of this study was to determine the effects of selective lesions of A2 neurons on the renal vasodilation and sympathoinhibition induced by hypertonic saline (HS) infusion. Male Wistar rats (280-350 g) received an injection into the NTS of anti-dopamine-beta-hydroxylase-saporin (A2 lesion; 6.3 ng in 60 nl; n = 6) or free saporin (sham; 1.3 ng in 60 nl; n = 7). Two weeks later, the rats were anesthetized (urethane 1.2 g⋅kg(-1) b.wt., i.v.) and the blood pressure, renal blood flow (RBF), renal vascular conductance (RVC) and renal sympathetic nerve activity (RSNA) were recorded. In sham rats, the HS infusion (3 M NaCl, 1.8 ml⋅kg(-1) b.wt., i.v.) induced transient hypertension (peak at 10 min after HS; 9±2.7 mmHg) and increases in the RBF and RVC (141±7.9% and 140±7.9% of baseline at 60 min after HS, respectively). HS infusion also decreased the RSNA (-45±5.0% at 10 min after HS) throughout the experimental period. In the A2-lesioned rats, the HS infusion induced transient hypertension (6±1.4 mmHg at 10 min after HS), as well as increased RBF and RVC (133±5.2% and 134±6.9% of baseline at 60 min after HS, respectively). However, in these rats, the HS failed to reduce the RSNA (115±3.1% at 10 min after HS). The extent of the catecholaminergic lesions was confirmed by immunocytochemistry. These results suggest that A2 noradrenergic neurons are components of the neural pathways regulating the composition of the extracellular fluid compartment and are selectively involved in hypernatremia-induced sympathoinhibition.

Several findings suggest that A1 noradrenergic neurons in the caudal ventrolateral medulla (CVLM) contribute to body fluid homeostasis and cardiovascular regulation. Recently we demonstrated that the renal vasodilation induced by infusion of hypertonic saline (HS) depends on the integrity of the A1 neurons. Here we determined the effect of lesions of these neurons on the inhibition of the renal sympathetic nerve activity (RSNA) induced by HS infusion. All experiments were performed in Wistar rats (280-350 g). A1 neurons were lesioned by microinjections of antidopamine-beta-hydroxylase-saporin (6.3 ng in 60 nl) into the CVLM (n=5), whereas sham rats received microinjections of free saporin (1.3 ng in 60 nl, H=10). Two weeks later, rats were anesthetized (urethane 1.2 g/kg, iv), and instrumented for recording of arterial pressure and RSNA. In sham rats, HS infusion (3 M NaCl, 0.18 ml/100 g bw, iv) induced a transient (<= 30 min) hypertension (peak at 10 min; 9 5 mm Hg) and a fall in RSNA (-32 +/- 7% of baseline at 10 min). A1-lesions increased the duration of the pressor response induced by HS infusion (16 +/- 2 mm Hg at 60 min) and abolished the fall in RSNA (-6 +/- 8% of baseline at 10 min). Catecholaminergic lesions extensions were confirmed by immunocytochemistry. Unilateral renal denervation reduced the renal vasodilatation induced by HS infusion (112 +/- 7% in denervated rats versus 127 +/- 4% in sham, 20 min after HS). These results Suggest that A1 noradrenergic neurons are involved in the sympathoinhibition and consequent renal vasodilatation to acute changes in the extracellular fluid compartment. (C) 2008 Elsevier B.V. All rights reserved.

Previous studies suggested that neurons located in the midline and adjacent regions of the caudal medulla participate in cardiovascular regulation. Presently we sought to determine the effects of chemical excitation or lesion of this area. Male Wistar rats were anesthetized, paralized, and artificially ventilated and prepared for mean arterial pressure (MAP), heart rate (HR), and blood flow (BF) recordings. Hindquarter (HQVC) and renal vascular conductance (RVC) were determined by the ratio MAP/BF. Bilateral microinjection of KA (5 Mm, 50 nL) into CPM (1.6 rostral, 0.5 lat and −2.3 mm to the CS) increased MAP (+43±10.3 mmHg), HR (+48±23.6 bpm) and induced renal and hindquarter vasoconstriction (−72±8.3; −75±3.6% of baseline, respectively). Reversely, bilateral microinjection of ibotenic acid (2.5nM, 50nL) induced hypotension (−41±13.3 mmHg) and bradicardia (−75±43.1 bmp) without significant changing RVC or HVC (2±12.8; 33±29.2% of baseline respectively). Forty minutes after IBO microinjection of KA into the same sites overturned these effects, inducing marked hypertension (+38±13.7 mmHg), tachycardia (43±8.3 bpm) and renal and hindlimb vasoconstriction (−74±5.9,−75±6.4% of baseline, respectively). These results suggested that paramedial medulla contains excitatory and inhibitory cardiovascular pathways that may be differentiated by their sensitivity to glutamate agonists.

GiDA stimulation produced sympathoinhibition and hypotension, while microinjections of kainic acid (KA) in this region produced increased levels of sympathetic nerve activity (SNA) and hypertension. The present study sought to determine whether the effects of KA in GiDA are dependent on either RVLM activity or forebrain projections. Recordings of arterial pressure (AP) and heart rate (HR) and postganglionic splanchnic SNA were made from male Sprague-Dawley rats (300–500 g) anesthetized with urethane/chloralose, paralyzed, and artificially ventilated. Bilateral microinjections of KA (20mM) into GiDA produced hypertension (154±11mmHg) and increased SNA to 175% of control. SNA remained elevated (201±51% of control) following a transection of the neuraxis between GiDA and RVLM (2.3 mm rostral to calamus scriptorius), although AP was reduced to 88±13 mmHg. In a separate group of animals, bilateral muscimol microinjections into the RVLM decreased SNA (−55±4% of control) and AP (54±6 mmHg). Under these conditions, KA into the GiDA increased SNA to 260±16% of control and AP to a peak of 167±8 mmHg. SNA was unchanged (257±16% of control) following a transection rostral to RVLM (3.5 mm rostral to calamus scriptorius), although AP was reduced to 80±12 mmHg. These results suggest that an increase in SNA and a hypertension can be induced by KA into the GiDA during muscimol inhibition of the RVLM and in the absence of connections between GiDA and forebrain structures. Financial support: CAPES.

Há mais de 30 anos foi proposto um modelo para explicar como o sistema nervoso central promove a regulação do sistema cardiovascular, onde os núcleos vasomotores do bulbo seriam as principais estruturas envolvidas no controle do reflexo cardiovascular. Segundo este modelo, o núcleo do trato solitário (NTS) é o primeiro núcleo a integrar as informações cardiovasculares vindas dos baroceptores e também parece integrar vias descendentes provenientes de núcleos superiores como o hipotálamo, importantes para as reações de alerta e defesa. Do NTS saem projeções excitatórias para a região caudoventrolateral (CVL) do bulbo, a qual inibe a região rostroventrolateral (RVL). Esta última região constitui a principal fonte de eferências excitatórias para os neurônios simpáticos pré-ganglionares (SPN), sendo responsável pelo tonus simpático para o coração e vasos. Projeções importantes do CVL para estruturas diencefálicas (núcleo preóptico mediano, núcleo paraventricular do hipotálamo e núcleo supraóptico) também estão envolvidas no controle da composição e/ou volume do compartimento extracelular. A área depressora gigantocelular (GiDA) constitui outro possível centro vasomotor envolvido nos ajustes de fluxo sangüíneo por meio de projeções diretas para o SPN. No entanto, o meio pelo qual a GiDA exerce seu efeito vasodepressor ainda é desconhecido. Nos últimos 10 anos, nosso laboratório tem se dedicado a deslindar as vias e mecanismos neurais associados à regulação do fluxo sangüíneo visceral e muscular. Resultados obtidos ao longo destes estudos resultaram em evidências que são incompatíveis com o modelo proposto.