Cardiovascular adjustments induced by hypertonic saline in hemorrhagic rats: Involvement of carotid body chemoreceptors

The peripheral hyperosmolarity elicited by intravenous infusion of hypertonic saline brings potential benefits to the treatment of hemorrhage. the neural mechanisms involved in these beneficial effects remain unknown. the present study examines the role of carotid chemoreceptors in cardiovascular responses induced by hypertonic saline after hypovolemic hemorrhage in rats. Male Wistar rats (300-400 g) were anesthetized with thiopental, and instrumented for recording of mean arterial pressure. Arterial pressure was reduced to 60 mm Hg by withdrawal of arterial blood over 10 min, and maintained at this level for 60 min by withdrawal or infusion of blood. in control rats (n = 8) with intact chemoreceptors, the subsequent intravenous infusion of hypertonic saline (3M NaCl, 1.8 ml kg(-1) body weight, in 2 min) restored blood pressure (pressure increased from 61 +/- 4 to 118 +/- 5 mm Hg). in experimental rats (n = 8), the carotid body arteries were tied, 30 min after the beginning of the hypotensive phase, leaving the carotid chemoreceptors ischemic. in these rats, hypertonic saline failed to restore blood pressure (pressure increased from 55 +/- 1 to 70 +/- 6 mm Hg). These findings suggest that the restoration of blood pressure after hypovolemic hemorrhage induced by hypertonic saline depends on intact carotid chemoreceptors. (C) 2010 Elsevier B.V. All rights reserved.Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Univ Fed Goias, Dept Physiol Sci, Inst Ciencias Biol 2, BR-74001970 Goiania, Go, BrazilUniversidade Federal de São Paulo, Dept Physiol, Escola Paulista Med, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Physiol, Escola Paulista Med, São Paulo, BrazilCAPES: BEX1380/07-9Web of Scienc

Impact of Oxidative Changes and Possible Effects of Genetics Polymorphisms of Glutathione S-Transferase in Diabetics Patients with Complications

Pancreatic β cells are more sensitive to cytotoxic stress than several other cells due to the expression of very low levels of antioxidant enzymes. Glutathione-S-transferase (GST) is a detoxification enzyme essential for a cellular protection against oxidative damage. Thus, the objective of this chapter is to verify the impact of the hypothesis of all effects of Glutathione S-transferase polymorphism in patients with diabetic complications. Diabetic nephropathy (DN) is the main secondary complication of diabetes mellitus (DM). Notably, the expression of GST genes has been described in different variations as ethnic populations. Some studies have suggested association between genetic polymorphism for GSTM1, GSTT1 and GSTP1 and DN, but others do not. The results are still inconsistent and, therefore, more studies are needed to be performed

The Effect of Nrf2 on Diabetic Complications

The Nrf2 has been identified as a key molecular player in orchestrating adaptive cellular interactions following a wide spectrum of cellular conditions that could be either extracellular or intracellular. The encoded transcription factor regulates genes, which contain antioxidant response elements (ARE) in their promoters; many of these genes encode proteins involved in response to environmental stress, detoxifying enzymes, metabolic enzymes, injury, and inflammation, which includes the production of free radicals. The association between oxidative stress and inflammation with progression of diabetic nephropathy and cardiomyopathy has been described. The prevention of diabetic nephropathy and cardiomyopathy has become a global concern for those who are working in diabetic care management. Therefore, activation of Nrf2 has the potential to protect against macromolecular damage. Studies have demonstrated the beneficial role of Nrf2 induction in the prevention of DN. Upon exposure of cells to oxidative stress or electrophilic compounds, Nrf2 dissociates from Keap1 and translocates into the nucleus to bind to antioxidant-responsive elements in the genes encoding antioxidant enzymes. Upregulation of these Nrf2-dependent antioxidants promotes detoxification and anti-inflammatory function. Thus, the Nrf2 activators have been suggested for preventing diabetic nephropathy

Bowman-Birk protease inhibitor from Vigna unguiculata seeds enhances the action of bradykinin-related peptides

The hydrolysis of bradykinin (Bk) by different classes of proteases in plasma and tissues leads to a decrease in its half-life. Here, Bk actions on smooth muscle and in vivo cardiovascular assays in association with a protease inhibitor, Black eyed-pea trypsin and chymotrypsin inhibitor (BTCI) and also under the effect of trypsin and chymotrypsin were evaluated. Two synthetic Bk-related peptides, Bk1 and Bk2, were used to investigate the importance of additional C-terminal amino acid residues on serine protease activity. BTCI forms complexes with Bk and analogues at pH 5.0, 7.4 and 9.0, presenting binding constants ranging from 103 to 104 M−1. Formation of BTCI-Bk complexes is probably driven by hydrophobic forces, coupled with slight conformational changes in BTCI. In vitro assays using guinea pig (Cavia porcellus) ileum showed that Bk retains the ability to induce smooth muscle contraction in the presence of BTCI. Moreover, no alteration in the inhibitory activity of BTCI in complex with Bk and analogous was observed. When the BTCI and BTCI-Bk complexes were tested in vivo, a decrease of vascular resistance and consequent hypotension and potentiating renal and aortic vasodilatation induced by Bk and Bk2 infusions was observed. These results indicate that BTCI-Bk complexes may be a reliable strategy to act as a carrier and protective approach for Bk-related peptides against plasma serine proteases cleavage, leading to an increase in their half-life. These findings also indicate that BTCI could remain stable in some tissues to inhibit chymotrypsin or trypsin-like enzymes that cleave and inactivate bradykinin in situ

A2 Noradrenergic Lesions Prevent Renal Sympathoinhibition Induced by Hypernatremia in Rats

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

ANSIEDAD, DEPRESIÓN Y ANÁLISIS NO LINEAL DE LA VARIABILIDAD DE LA FRECUENCIA CARDÍACA EN MIEMBROS DE EDUCACIÓN SUPERIOR

A análise não linear da Variabilidade da Frequência Cardíaca (VFC) é uma potencial ferramenta de correlação entre estados fisiológicos e emocionais. O objetivo deste estudo foi correlacionar alterações nos parâmetros não lineares da VFC com índices de ansiedade e depressão em ingressantes no ensino superior na Universidade Federal de Goiás (UFG). Para o registro da VFC, foi utilizado o Frequencímetro Polar® modelo RS800cx (Electro Oi, Finland).  Para  análise dos níveis de depressão, foi utilizado o Inventário de Depressão de Beck (BDI), e para análise da ansiedade, os Inventários de Ansiedade Traço e Estado (IDATE T e E). Ao todo, 50 (19,4±2,48 anos) voluntários participaram do estudo. Os scores dos inventários de depressão e ansiedade apontaram que o público apresentou índices baixos e moderados de ambas as condições, respectivamente. Foram encontradas correlações estatisticamente significativas entre o parâmetro SD2 (oriundo do Plot de Poincaré na análise da VFC), dados de entropia (ApEn e SampEn) e de propriedade fractal (DFA:?1) e os níveis de ansiedade traço e estado. Embora ApEn e SampEn ainda não apresentem correspondências fisiológicas bem definidas, DFA:?1 tem sido associado a modulação parassimpática da frequência cardíaca. Assim sendo, conclui-se que estados emocionais negativos crônicos, como em transtornos de ansiedade e humor, podem ser acompanhados por incremento parassimpático na VFC, pois assim o organismo seria capaz de não se desgastar contra estressores de longa duração. Novos estudos são necessários para a melhor compreensão das bases fisiológicas e evolutivas da depressão e da ansiedade.The non-linear analysis of the heart rate variability (HRV) is a potential correlation tool between physiological and emotional states.                                The aim of this study was correlate changes in non-linear parameters of the HRV with anxiety and depression indices in higher education entrants from Federal University of Goiás (UFG). To record HRV, the Polar Frequency Metermodel Polar® RS800cx (Electro Oi, Finland) was used. To analyze the levels of depression, the Beck Depression Inventory-I (BDI) was used, and for analysis of anxiety, the Inventories of State and Trace (IDATE T and E). Altogether, 50 (19.4±2.48 years) volunteers participated in the study. The scores of the depression and anxiety inventories indicated that the public had low and moderate indices of both conditions, respectively. Statistically significant correlations were found between the SD2 parameter (from the Poincaré plot in the HRV analysis), entropy data (ApEn and SampEn) and fractal property (DFA: ?1) and trait and state anxiety levels. Although ApEn e SampEn still do not have well-defined physiological correspondences, DFA: ?1 has been associated with parasympathetic modulation of heart rate. Therefore, it is concluded that chronic negative emotional states, such as anxiety and humor disorders, can be accompanied by parasympathetic increase in HRV, so the organism would be able to not wear out against long-term stressors. New studies are necessary to understand the physiological and evolutional bases of depression and anxiety.El análisis no lineal de la variabilidad de la frecuencia cardíaca (VFC) es una herramienta potencial para correlacionar estados fisiológicos y emocionales. El propósito de este estudio. es correlacionar los cambios en los parámetros no lineales de VFC con las tasas de ansiedad y depresión en aquellos que ingresan a la educación superior en la Universidad Federal de Goiás (UFG). Para la grabación de VFC, se obtuvieron latidos por latidos del medidor de frecuencia Polar® modelo RS800cx (Electro Oi, Finlandia). Para analizar los niveles de depresión, se usó el Inventario de Depresión de Beck (BDI) y para el análisis de ansiedad, los Inventarios de Rasgos y Ansiedad Estatal (STAI T y E). En total, 50 (19,4±2,48 años). Los puntajes de los inventarios de depresión y ansiedad mostraron que el público tenía tasas bajas y moderadas de ambas afecciones, respectivamente. Se encontraron correlaciones estadísticamente significativas entre los parámetros de entropía (ApEn y SampEn) y la propiedad fractal (DFA: ?1) y los niveles de rasgo y ansiedad de estado. Aunque ApEn y SampEn todavía no tienen correspondencias fisiológicas bien definidas, DFA: ?1 se ha asociado con la modulación parasimpática de la frecuencia cardíaca. Por lo tanto, se concluye que los estados emocionales negativos crónicos, como en los trastornos de ansiedad y estado de ánimo, pueden ir acompañados de un aumento parasimpático, ya que de esta manera el cuerpo podría almacenar energía y no desgastarse contra eventos estresantes a largo plazo. Se necesitan más estudios para comprender mejor las bases fisiológicas y evolutivas de la depresión y la ansiedad

Role of the Carotid Bodies in the Hypertensive and Natriuretic Responses to NaCl Load in Conscious Rats

Hyperosmotic challenges trigger a hypertensive response and natriuresis mediated by central and peripheral sensors. Here, we evaluated the importance of the carotid bodies for the hypertensive and natriuretic responses to acute and sub-chronic NaCl load in conscious rats. Male Wistar rats (250–330 g) submitted to bilateral carotid body removal (CBX) or sham surgery were used. One day after the surgery, the changes in arterial blood pressure (n = 6–7/group) and renal sodium excretion (n = 10/group) to intravenous infusion of 3 M NaCl (1.8 mL/kg b.w. during 1 min) were evaluated in non-anesthetized rats. Another cohort of sham (n = 8) and CBX rats (n = 6) had access to 0.3 M NaCl as the only source of fluid to drink for 7 days while ingestion and renal excretion were monitored daily. The sodium balance was calculated as the difference between sodium infused/ingested and excreted. CBX reduced the hypertensive (8 ± 2 mmHg, vs. sham rats: 19 ± 2 mmHg; p < 0.05) and natriuretic responses (1.33 ± 0.13 mmol/90 min, vs. sham: 1.81 ± 0.11 mmol/90 min; p < 0.05) to acute intravenous infusion of 3 M NaCl, leading to an increase of sodium balance (0.38 ± 0.11 mmol/90 min, vs. sham: -0.06 ± 0.10 mmol/90 min; p < 0.05). In CBX rats, sub-chronic NaCl load with 0.3 M NaCl to drink for 7 days increased sodium balance (18.13 ± 4.45 mmol, vs. sham: 5.58 ± 1.71 mmol; p < 0.05) and plasma sodium concentration (164 ± 5 mmol/L, vs. sham: 140 ± 7 mmol/L; p < 0.05), without changing arterial pressure (121 ± 9 mmHg, vs. sham: 116 ± 2 mmHg). These results suggest that carotid bodies are important for the maintenance of the hypertensive response to acute hypertonic challenges and for sodium excretion to both acute and chronic NaCl load

Role for A1 noradrenergic neurons in cardiovascular and behavioral responses induced by acute changes in circulating volume and composition

A integridade celular depende essencialmente da manutenção da composição e do volume do compartimento extracelular dentro de uma faixa de variação restrita. Alterações do volume e/ou da composição do compartimento extracelular são detectadas pelo sistema nervoso central (SNC) através de sinal provenientes principalmente dos osmoreceptores centrais e periféricos, dos baroceptores e dos receptores cardiopulmonares. Uma vez ativado, o SNC modula respostas cardiovasculares, endócrinas, renais e comportamentais específicas, que visam restabelecer as condições volêmicas fisiológicas. Neste estudo, tivemos como objetivos determinar: 1. as vias centrais envolvidas nas respostas cardiovasculares induzidas por variações no volume e/ou na composição do compartimento extracelular; 2. as vias centrais envolvidas nas respostas comportamentais induzidas por variações no volume e/ou na composição do compartimento extracelular. Para tanto, ratos Wistar (280-350g) foram anestesiados com uretana (1 ,2 g/kg, iv.) após a indução com halotano (2 por cento em 02 100 por cento) e submetidos a três (3) diferentes manipulações centrais: 1. lesão da região AV3V; 2. bloqueio dos adrenoceptores a1 localizado no MePO ou; 3. a lesão especifica do grupamento noradrenérgico A1. Para o registro dos parâmetros cardiovasculares analisados, estes animais submetidos à canulação da veia jugular direita, artéria e veia femoral esquerdas para infusão de NaCI 3M (0,18m1/100g de massa corpórea) ou Ficoll 4 por cento (1 por cento da massa corpórea, na taxa de infusão de 0,4m1/min), registro de pressão arterial média (PAM) e infusão de anestésico, respectivamente. O fluxo sangüíneo renal (FSR) foi obtido por fluxometria ultra sônica e expresso como porcentagem do basal. A condutância vascular renal (CR) foi calculada como a razão FSR/PAM e expressa como porcentagem do basal. Os resultados obtidos demonstram que em …(au).BV UNIFESP: Teses e dissertaçõe

Role of the medullary regions on circulating volume and blood pressure regulation: from physiological states to hypertension from physiological states to hypertension

The present study sought to characterize mechanisms and neural pathways involved in the regulation of volume and composition of the extracellular compartment and the participation of the rostroventral region of the medulla oblongata (RVLM) in the arterial hypertension induced by chronic administration of angiotensin II combined with a high sodium diet. The first part sought to determine the participation of humoral and autonomic mechanisms in the cardiovascular and renal effects induced by a sodium load and the role of the noradrenergic A1 and A2 groups in the autonomic changes induced by a sodium load. Wistar rats (280 – 350 g) were anesthetized with urethane (1.2  Kg-1, i.v.) or sodium thiopental (40 mg  Kg-1, i.v.) and prepared for collection of urine and recording of mean arterial pressure (MAP), renal blood flow (RBF), renal vascular conductance (RC), and renal sympathetic activity (RSA). In an additional series of experiments, the noradrenergic A1 group in the caudolateral medulla oblongata (CVLM) or the A2 group in the nucleus of the solitary tract (NTS) were lesioned by nanoinjection of anti-DH (0.105 ng  nl-1 in 60 nl). In anethetized rats, an acute load of sodium (3 M NaCl, 1.8 ml Kg-1, i.v.) caused prolonged increases of RBF and RC, indicating renal vasodilation. In animals subjected to renal denervation or blockade of oxytocin receptors (Atosiban; atosiban acetate, 40 mg  Kg-1  h-1, i.v.), the renal vasodilation induced by hypernatremia was significantly less than in the control group. In animals subjected to both renal renervation and infusion of Atosiban, the sodium load failed to significantly change renal conductance. Control rats excreted 87% of the administered sodium load within 90 min. Sodium excretion was slightly reduced in Atosiban-treated animals (69% in 90 min), and sodium excretion was very low in renal denervated rats treated with Atosiban (29% in 90 min). Hypernatremia caused renal sympathoinhibition, which was completely abolished by lesions of the A1 and A2 groups. Animals with A2 lesions also showed a small reduction in the renal vasodilation induced by hypernatremia. These results indicate that the renal vasodilation and natriuresis induced by hypernatremia depend on both neural and humoral mechanisms, and that the noradrenergic A1 and A2 groups are involved in the sympatho-inhibition induced by hypernatremia. The second part of this thesis investigates the role of sympathetic pre-motor neurons in the RVLM in the hypertension induced by Ang II and a high-sodium diet. Sprague-Dawley rats (350-450 g) were divided in two groups. The hypertensive group was maintained for 45 days on a high-sodium diet (2% NaCl) and received a subcutaneous infusion of Ang II (150 ng kg-1 min-1) during the final 15 days of this period. The normotensive group was kept on a diet with 0.4% NaCl and received a subcutaneous infusion with saline (0.15% NaCl). After 15 days of infusion, the rats were anesthetized with urethane (700 mg kg-1, i.v.) and -cloralose (70 mg kg-1, i.v.) and prepared for measurement of mean arterial pressure (MAP), heart rate (HR), phrenic nerve activity, and extracellular recording of RVLM neurons. The results show that all the neurons that were recorded were of the bulbospinal sympatho-exitatory type. Spontaneous firing rates were higher in hypertensive animals than in normotensive controls. Two different populations of vasomotor neurons could be identified in this region. A population of neurons that were inhibited by baroreceptor activation and whose activity was locked to the cardiac cycle had similar firing rates in hypertensive and normotensive rats. A population of neurons that were inhibited by baroreceptor activation but whose activity was not locked to the cardiac cycle was much more active (142%) in hypertensive than in normotensive rats. The increase in MAP needed to silence these neurons was higher in hypertensive animals, and the firing rate observed during baroreceptor unloading was higher. This population of neurons contained tonically active and bursting neurons. Only phasically active neurons were hyperactive in hypertensive rats. Activity of these phasically active neurons was locked to the respiratory cycle, and depended on central mechanisms, and not on respiratory movements. These results suggest that treatment with angiotensin and a high-sodium diet causes arterial hypertension and increases spontaneous firing in a subpopulation of RVLM neurons with strictly identified functional characteristics. It is possible that hyperactivity of these neurons contributes to sympathetic activation and hypertension induced by this experimental model.Este trabalho visou a caracterizar alguns mecanismos e vias neurais envolvidas na regulação do volume e da composição do compartimento extracelular e a participação da região rostroventrolateral da medula oblongata (RVLM) na hipertensão arterial induzida pela administração crônica de angiotensina II associada a dieta hipersódica. Na primeira parte buscamos determinar a participação de mecanismos humorais e autonômicos nos ajustes cardiovasculares e renais induzidos pela sobrecarga de sódio e a participação dos grupamentos noradrenérgicos A1 e A2 nos ajustes autonômicos induzidos pela sobrecarga de sódio. Ratos Wistar (280-350g) anestesiados com uretana (1,2 g - Kg-1, i.v.) ou tiopental sódico (40 mg - Kg-1, i.v.) foram instrumentados para a coleta de urina e os registros da pressão arterial média (PAM), freqüência cardíaca (FC), fluxo sanguíneo renal (FSR), condutância vascular renal (CR) e atividade simpática renal (ASR). Em outra série de experimentos, animais foram submetidos a lesão dos grupamentos noradrenérgicos através da nanoinjeção de saporina-anti-DH (0,105 ng - nl-1 em 60 nl) na região caudoventrolateral da medula oblongata (CVLM; grupamento A1) ou no núcleo do trato solitário (NTS; grupamento A2). Em ratos anestesiados a sobrecarga aguda de sódio (NaCl 3 M, 1,8 ml Kg-1, i.v.) promoveu aumentos mantidos do FSR e da CR, indicando vasodilatação renal. Em animais previamente submetidos a desnervação renal (DR) ou ao bloqueio dos receptores de ocitocina (Atosiban; acetato de atosibana, 40 mg - Kg-1 - h-1, i.v.), a vasodilatação renal induzida pela hipernatremia foi significativamente menor do que a observada no grupo controle. Em animais submetidos a DR e a administração do Atosiban não foram observadas variações significativas do FSR e da CR após a infusão, indicando que a vasodilatação renal induzida pela hipernatremia foi completamente abolida nestes animais. Nos animais do grupo controles também foi observado que 87% do sódio administrado foi excretado até 90 min após a infusão de salina hipertônica. Nos animais tratados com Atosiban, observa-se redução discreta da natriurese induzida (69%). Em animais submetidos a DR e Atosiban, apenas 29% do sódio infundido havia sido excretado após 90 min. Nos animais submetidos a lesão dos grupos A1 ou A2 foi observado que a simpato-inibição em resposta a hipernatremia observada nos animais controles foi completamente abolida. Em animais com lesão do grupamento A2 observa-se também redução discreta na vasodilatação renal induzida pela hipernatremia. Estes resultados indicam que a vasodilatação renal e a excreção de sódio induzida por hipernatremia dependem de mecanismos neurais e humorais e que neurônios noradrenérgicos dos grupos A1 e A2 estão envolvidos nas respostas simpato-inibitórias induzidas pela hipernatremia. Na segunda parte deste trabalho buscamos avaliar a participação dos neurônios pré-motores simpáticos do RVLM na hipertensão experimental induzida por Ang II e dieta hipersódica Ratos Sprague-Dawley (350-450 g) foram divididos em dois grupos: no grupo hipertenso (Ang II-Sal) os animais foram mantidos um período de 45 dias em uma dieta hipersódica (NaCl 2%) e receberam a administração subcutânea de Ang II (150 ng kg-1 min-1) nos últimos 15 dias. No grupo normotenso, os animais foram mantidos em dieta normossódica (0,4 % NaCl) e submetidos a administração subcutânea de soro fisiológico (NaCl 0,15%). Quinze dias após o inicio do tratamento os animais foram anestesiados com uretana (700 mg kg-1, i.v.) e -cloralose (70 mg kg-1, i.v.) e instrumentados para o registros da pressão arterial média (PAM), freqüência cardíaca (FC), atividade do nervo frênico e atividade dos neurônios da região RVLM. Os resultados demonstram que todos os neurônios registrados na RVLM apresentavam características de neurônios bulboespinais simpatoexcitatórios. A atividade espontânea dos neurônios registrados no grupo hipertenso era maior do que a observada em animais controle. A análise funcional identificou duas subpopulações de neurônios na RVLM: uma caracterizada por apresentar sincronismo cardíaco e ser barosensível. Nesta população a atividade neuronal espontânea encontrava-se semelhante entre os grupos controles e com hipertensão Ang II-Sal. A segunda subpopulação também era barosensível, mas não possuía atividade sincronizada com o ciclo cardíaco. Nesta subpopulação a freqüência espontânea de disparos foi significativamente maior (142%) nos animais com hipertensão Ang II-Sal do que no grupo controle. O aumento da PAM necessário para inibição destes neurônios e a freqüência máxima durante a desativação dos baroceptores foram significativamente maior no grupo hipertenso do que no grupo controle. Nesta subpopulação foram identificados dois padrões de descarga: um tônico e outro em surtos. Apenas nos neurônios com descarga em surtos a atividade espontânea se encontrava aumentada no grupo hipertenso quando comparada ao controle. Por fim, foi evidenciado que o padrão em surtos encontrava-se em sincronismo com o ciclo respiratório, sendo esta modulação de origem central. Estes resultados sugerem que o tratamento Ang II e Sal promove hipertensão arterial e aumento da atividade espontânea numa subpopulação de neurônios da RVLM com características funcionais específicas. É possível que a hiperatividade destes neurônios possa estar relacionada com os aumentos da atividade simpática e da pressão arterial evidenciados neste modelo de hipertensão experimental.TEDEBV UNIFESP: Teses e dissertaçõe

Blockade of alpha 1-adrenoceptors in the median preoptic (MePO) nucleus impairs cardiovascular responses induced by intravenous hypertonic saline (HS) infusion

UNIFESP, EPM, Dept Physiol, BR-04023060 Sao Paulo, BrazilUNIFESP, EPM, Dept Physiol, BR-04023060 Sao Paulo, BrazilWeb of Scienc