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Search Results: 1 - 10 of 21 matches for " Lusiane Bendhack "
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Vasodilatation induced by forskolin involves cyclic GMP production  [PDF]
Mário dos Anjos Neto, Claure Nain Lunardi, Gerson Jhonatan Rodrigues, Lusiane Maria Bendhack
Journal of Biophysical Chemistry (JBPC) , 2011, DOI: 10.4236/jbpc.2011.24042
Abstract: Endothelium-derived relaxing factors contribute to smooth muscle relaxation. The aim of the present study was to investigate the contribution of nitric oxide (NO) produced in the endothelial cells to the vasodilatation stimulated with forskolin in rat aorta. Forskolin that directly activates adenylyl-cyclase, induced complete relaxation in phenylephrine-contracted aortas. Endothelium removal reduced the potency (pEC50) of forskolin without changes in the maximum effect (Emax). However, the inhibitor of endothelial NO-synthase (10 μM L- NG-Nitroarginine, L-NNA) reduced both Emax and pEC50 in intact endothelium aortic rings. L-NNA or L-NNA plus cyclooxygenase inhibitor indomethacin (10 μM) reduced both Emax and pEC50 of forskolin. Forskolin increased both the cytosolic Ca+2 concentration and the cytosolic NO concentration ([NO]c) in the endothelial cells. The PKA inhibitor KT5720 reduced the NO production activated by forskolin in the endothelial cells. The enhanced [NO]c in the endothelial cells increased cyclic guanosine-monophosphate (cGMP) in smooth muscle cells, which was abolished by L-NNA. Taken together, our results indicate that vasodilatation mediated by forskolin in rat aortic rings is potentiated by NO production in endothelial cells that increases the cGMP levels in the smooth muscle cells that along with cAMP contribute to the vasodilatation.
Tityus serrulatus venom and its toxins Ts1 and Ts5 increase cytosolic Ca2+ concentration in isolated vascular smooth muscle cells  [PDF]
Mário dos A. Neto, Flávio Vasconcelos, Lusiane M. Bendhack, Eliane C. Arantes
Journal of Biophysical Chemistry (JBPC) , 2012, DOI: 10.4236/jbpc.2012.34035
Abstract: Voltage-gated Na+ channel (Nav channel) scorpion toxins are classified as α- and β-neurotoxins. Ts5 (α-neurotoxin) and Ts1 (β-neurotoxin) from Tityus serrulatus venom (TsV) interact with Nav channels, increasing Na+ influx and activating voltage-dependent Ca2+ channels. This study aimed to investigate the effect of TsV, Ts1 and Ts5 on the cytosolic Ca2+ concentration ([Ca2+]C) in rat aortic smooth muscle cells. Toxins were isolated by ion exchange chromatography (Ts1) followed by RP-HPLC (Ts5). The rat aortic smooth muscle cells were isolated in Hanks buffer pH 7.4 and loaded with 5 μmol/L of Fura-2AM (45 minutes at 37℃), in order to measure [Ca2+]C by fluorescence of Fura-2/AM (ratio 340/380 nm). The fluorescence was measured in one single cell (excitation: 340 and 380 nm; emission: 510 nm). TsV (100 and 500 mg/mL) and its toxins Ts1 and Ts5 (50 and 100 mg/mL each) led to a concentration-dependent increase in [Ca2+]C. Tetrodotoxin (1 mmol/L), a Nav channel blocker, and verapamil (1 mmol/L), a voltage-operated Ca2+ channel blocker, inhibited the increase in [Ca2+]C induced by TsV (500 mg/mL). In conclusion, TsV and its toxins induce a concentration-dependent increase in [Ca2+]C that probably occurs through interaction with Nav channels, thus inducing depolarization and consequent Ca2+ influx. This assumption is based on the fact that this effect is inhibited by tetrodotoxin and verapamil, showing a direct action of TsV toxins on aorta smooth muscle cells.
Role of endothelium on the abnormal Angiotensin-mediated vascular functions in epileptic rats  [PDF]
Carolina Restini, Rosana Reis, Claudio Costa-Neto, Norberto Garcia-Cairasco, José Cortes-de-Oliveira, Lusiane Bendhack
Journal of Biophysical Chemistry (JBPC) , 2012, DOI: 10.4236/jbpc.2012.32019
Abstract: Epidemiological studies have found that the risk for cardiovascular disease is increased in patients with epilepsy. The Renin Angiontensin System (RAS), an important player in vascular tone control, is also involved in many neurological disorders, including seizures and epilepsy. Although it has been reported that Angiotensin II (Ang II) release and Angiotensin receptors expression are altered in many cerebral areas in patients/animal models with neurological disorders, there are no data on the vascular function. We evaluated Ang I and Ang II-mediated vascular responses and to correlate their contractile responses to the pres- ence of endothelium and the protein levels of components of the RAS (AT1, AT2, Mas and ACE) in aorta isolated from genetically epileptic rats (WAR strain). The major finding was that the vascular contractile response induced by Ang I and Ang II is endothelium-dependent. Ang II induced contractions in aortas from Wistar rats either with intact endothelium (E+) (1.16 ± 0.04 g, n = 6) and endothelium-denuded (E-) (1.24 ± 0.04 g, n = 6). Maximum contractile response (ME) induced by Ang I was lower in Wistar E+ (0.45 ± 0.03 g, n = 6) compared with Wistar E- (1.13 ± 0.08 g, n = 6). Ang I and Ang II failed to induce contraction in WAR E+, whereas the ME induced by Ang I in WAR E- was lower (0.52 ± 0.04 g, n = 11) than in the Wistar. ME induced by Ang II in aortas from WAR was also lower (0.40 ± 0.03 g, n = 11) compared with Wistar. AT1 receptor expression in both E+ WAR and Wistar was lower than in both E- WAR and Wistar. AT2 and Mas receptor expression was higher in Wistar E- and E+ as compared to WAR E- and E+. ACE expression was higher in both E+ WAR and Wistar, but it was lower in both E- WAR and Wistar. Endothelium impairs the contractile response induced by Angiotensin in WAR, suggesting that endothelial relaxing factors play important role on the aorta contraction.
The Effect of Extracellular pH Changes on Intracellular pH and Nitric Oxide Concentration in Endothelial and Smooth Muscle Cells from Rat Aorta
Verena K. Capellini, Carolina B. A. Restini, Lusiane M. Bendhack, Paulo R. B. Evora, Andréa C. Celotto
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0062887
Abstract: Aims It has been known for more than a century that pH changes can alter vascular tone. However, there is no consensus about the effects of pH changes on vascular response. In this study, we investigated the effects of extracellular pH (pHo) changes on intracellular pH (pHi) and intracellular nitric oxide concentration ([NO]i) in freshly isolated endothelial cells and cross sections from rat aorta. Main Methods The HCl was used to reduce the pHo from 7.4 to 7.0 and from 7.4 to 6.5; the NaOH was used to increase the pHo from 7.4 to 8.0 and from 7.4 to 8.5. The fluorescent dyes 5-(and-6)-carboxy SNARF-1, acetoxymethyl ester, acetate (SNARF-1) and diaminofluorescein-FM diacetate (DAF-FM DA) were employed to measure the pHi and [NO]i, respectively. The fluorescence intensity was measured in freshly isolated endothelial cells by flow cytometry and in freshly obtained aorta cross sections by confocal microscopy. Key Findings The endothelial and vascular smooth muscle pHi was increased at pHo 8.5. The extracellular acidification did not change the endothelial pHi, but the smooth muscle pHi was reduced at pHo 7.0. At pHo 8.5 and pHo 6.5, the endothelial [NO]i was increased. Both extracellular alkalinization and acidification increased the vascular smooth muscle [NO]i. Significance Not all changes in pHo did result in pHi changes, but disruption of acid-base balance in both directions induced NO synthesis in the endothelium and/or vascular smooth muscle.
Vascular Relaxation Induced by C-Type Natriuretic Peptide Involves the Ca2+/NO-Synthase/NO Pathway
Fernanda A. Andrade, Carolina B. A. Restini, Marcella D. Grando, Leandra N. Z. Ramalho, Lusiane M. Bendhack
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0095446
Abstract: Aims C-type natriuretic peptide (CNP) and nitric oxide (NO) are endothelium-derived factors that play important roles in the regulation of vascular tone and arterial blood pressure. We hypothesized that NO produced by the endothelial NO-synthase (NOS-3) contributes to the relaxation induced by CNP in isolated rat aorta via activation of endothelial NPR-C receptor. Therefore, the aim of this study was to investigate the putative contribution of NO through NPR-C activation in the CNP induced relaxation in isolated conductance artery. Main Methods Concentration-effect curves for CNP were constructed in aortic rings isolated from rats. Confocal microscopy was used to analyze the cytosolic calcium mobilization induced by CNP. The phosphorylation of the residue Ser1177 of NOS was analyzed by Western blot and the expression and localization of NPR-C receptors was analyzed by immunohistochemistry. Key Findings CNP was less potent in inducing relaxation in denuded endothelium aortic rings than in intact ones. L-NAME attenuated the potency of CNP and similar results were obtained in the presence of hydroxocobalamin, an intracellular NO0 scavenger. CNP did not change the phosphorylation of Ser1177, the activation site of NOS-3, when compared with control. The addition of CNP produced an increase in [Ca2+]c in endothelial cells and a decrease in [Ca2+]c in vascular smooth muscle cells. The NPR-C-receptors are expressed in endothelial and adventitial rat aortas. Significance These results suggest that CNP-induced relaxation in intact aorta isolated from rats involves NO production due to [Ca2+]c increase in endothelial cells possibly through NPR-C activation expressed in these cells. The present study provides a breakthrough in the understanding of the close relationship between the vascular actions of nitric oxide and CNP.
Deficient Regulatory T Cell Activity and Low Frequency of IL-17-Producing T Cells Correlate with the Extent of Cardiomyopathy in Human Chagas' Disease
Paulo Marcos Matta Guedes equal contributor,Fredy Roberto Salazar Gutierrez equal contributor,Grace Kelly Silva,Renata Dellalibera-Joviliano,Gerson Jhonatan Rodrigues,Lusiane Maria Bendhack,Anis Rassi Jr,Anis Rassi,André Schmidt,Benedito Carlos Maciel,José Antonio Marin Neto,Jo?o Santana Silva
PLOS Neglected Tropical Diseases , 2012, DOI: 10.1371/journal.pntd.0001630
Abstract: Background Myocardium damage during Chagas' disease results from the immunological imbalance between pro- and production of anti-inflammatory cytokines and has been explained based on the Th1–Th2 dichotomy and regulatory T cell activity. Recently, we demonstrated that IL-17 produced during experimental T. cruzi infection regulates Th1 cells differentiation and parasite induced myocarditis. Here, we investigated the role of IL-17 and regulatory T cell during human Chagas' disease. Methodology/Principal Findings First, we observed CD4+IL-17+ T cells in culture of peripheral blood mononuclear cells (PBMC) from Chagas' disease patients and we evaluated Th1, Th2, Th17 cytokine profile production in the PBMC cells from Chagas' disease patients (cardiomyopathy-free, and with mild, moderate or severe cardiomyopathy) cultured with T. cruzi antigen. Cultures of PBMC from patients with moderate and severe cardiomyopathy produced high levels of TNF-α, IFN-γ and low levels of IL-10, when compared to mild cardiomyopathy or cardiomyopathy-free patients. Flow cytometry analysis showed higher CD4+IL-17+ cells in PBMC cultured from patients without or with mild cardiomyopathy, in comparison to patients with moderate or severe cardiomyopathy. We then analyzed the presence and function of regulatory T cells in all patients. All groups of Chagas' disease patients presented the same frequency of CD4+CD25+ regulatory T cells. However, CD4+CD25+ T cells from patients with mild cardiomyopathy or cardiomyopathy-free showed higher suppressive activity than those with moderate and severe cardiomyopathy. IFN-γ levels during chronic Chagas' disease are inversely correlated to the LVEF (P = 0.007, r = ?0.614), while regulatory T cell activity is directly correlated with LVEF (P = 0.022, r = 0.500). Conclusion/Significance These results indicate that reduced production of the cytokines IL-10 and IL-17 in association with high levels of IFN-γ and TNF-α is correlated with the severity of the Chagas' disease cardiomyopathy, and the immunological imbalance observed may be causally related with deficient suppressor activity of regulatory T cells that controls myocardial inflammation.
High concentrations of KCl release noradrenaline from noradrenergic neurons in the rat anococcygeus muscle
Araujo, C.B.L.;Bendhack, L.M.;
Brazilian Journal of Medical and Biological Research , 2003, DOI: 10.1590/S0100-879X2003000100013
Abstract: the aim of the present study was to investigate the effects of high concentrations of kcl in releasing noradrenaline from sympathetic nerves and its actions on postsynaptic a-adrenoceptors. we measured the isotonic contractions induced by kcl in the isolated rat anococcygeus muscle under different experimental conditions. the contractile responses induced by kcl were inhibited by a-adrenoceptor antagonists in 2.5 mm ca2+ solution. prazosin reduced the maximum effect from 100 to 53.9 ± 10.2% (p<0.05) while the pd2 values were not changed. the contractile responses induced by kcl were abolished by prazosin in ca2+-free solution (p<0.05). treatment of the rats with reserpine reduced the maximum effect induced by kcl as compared to the contractile responses induced by acetylcholine from 339.5 ± 157.8 to 167.3 ± 65.5% (p<0.05), and increased the pd2 from 1.57 ± 0.01 to 1.65 ± 0.006 (p<0.05), but abolished the inhibitory effect of prazosin (p<0.05). in contrast, l-name increased the contractile responses induced by 120 mm kcl by 6.2 ± 2.3% (p<0.05), indicating that kcl could stimulate the neurons that release nitric oxide, an inhibitory component of the contractile response induced by kcl. our results indicate that high concentrations of kcl induce the release of noradrenaline from noradrenergic neurons, which interacts with a1-adrenoceptors in smooth muscle cells, producing a contractile response in 2.5 mm ca2+ (100%) and in ca2+-free solution, part of which is due to a direct effect of kcl on the rat anococcygeus muscle.
Pr vention des Prostatakarzinoms: Was ist anders nach der REDUCE-Studie?
Schmitz-Dr?ger BJ,Bendhack M,D?rsam J
Blickpunkt der Mann , 2009,
Abstract:
Pneumonite intersticial em paciente sob tratamento com leflunomide: toxicidade da droga?
Reichert Jonatas,Reichert Adriane,Bendhack Luci Iolanda,Noronha Lucia de
Jornal de Pneumologia , 2003,
Abstract: O leflunomide é uma droga anti-reumática com a o imunomoduladora. Pneumonia intersticial granulomatosa nunca foi descrita com o uso de leflunomide. Relata-se o caso de uma mulher de 33 anos que apresentou dor torácica, emagrecimento e síndrome infecciosa respiratória no quinto mês de monoterapia com leflunomide para artrite reumatóide, progredindo para insuficiência respiratória no sexto mês. A radiografia de tórax revelou infiltrado pulmonar intersticial e alveolar bilateral predominando em lobos superior e médio, micronódulos esparsos e ausência de altera es mediastinais. Suspendeu-se o leflunomide. Após a resolu o da infec o persistiram les es intersticiais retículo-nodulares predominantemente na periferia dos ter os superiores do pulm o direito e ter o médio do pulm o esquerdo, entremeadas por padr o de vidro fosco em lobos superiores. Biópsia pulmonar a céu aberto revelou granulomas tuberculóides sem necrose central. Foi realizada extensa investiga o etiológica, que resultou negativa. Ocorreu resolu o espontanea do quadro após quatro meses. O quadro sugere que as manifesta es pulmonares neste caso foram causadas pelo leflunomide.
High concentrations of KCl release noradrenaline from noradrenergic neurons in the rat anococcygeus muscle
Araujo C.B.L.,Bendhack L.M.
Brazilian Journal of Medical and Biological Research , 2003,
Abstract: The aim of the present study was to investigate the effects of high concentrations of KCl in releasing noradrenaline from sympathetic nerves and its actions on postsynaptic alpha-adrenoceptors. We measured the isotonic contractions induced by KCl in the isolated rat anococcygeus muscle under different experimental conditions. The contractile responses induced by KCl were inhibited by alpha-adrenoceptor antagonists in 2.5 mM Ca2+ solution. Prazosin reduced the maximum effect from 100 to 53.9 ± 10.2% (P<0.05) while the pD2 values were not changed. The contractile responses induced by KCl were abolished by prazosin in Ca2+-free solution (P<0.05). Treatment of the rats with reserpine reduced the maximum effect induced by KCl as compared to the contractile responses induced by acetylcholine from 339.5 ± 157.8 to 167.3 ± 65.5% (P<0.05), and increased the pD2 from 1.57 ± 0.01 to 1.65 ± 0.006 (P<0.05), but abolished the inhibitory effect of prazosin (P<0.05). In contrast, L-NAME increased the contractile responses induced by 120 mM KCl by 6.2 ± 2.3% (P<0.05), indicating that KCl could stimulate the neurons that release nitric oxide, an inhibitory component of the contractile response induced by KCl. Our results indicate that high concentrations of KCl induce the release of noradrenaline from noradrenergic neurons, which interacts with alpha1-adrenoceptors in smooth muscle cells, producing a contractile response in 2.5 mM Ca2+ (100%) and in Ca2+-free solution, part of which is due to a direct effect of KCl on the rat anococcygeus muscle.
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