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1192. Nitric oxide synthase in pulmonary hypertension: lessons from knockout mice
- Creator:
- Fagan, K. A., McMurtry, I., and Rodman, D. M.
- Format:
- print, bez média, and svazek
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, oxid dusnatý, plicní hypertenze, nitric oxide, pulmonary hypertension, knockout mice, pulmonary vasoreactivity, vascular remodeling, 14, and 612
- Language:
- English
- Description:
- Nitric oxide (NO) is implicated in a wide variety of biological roles. NO is generated from three nitric oxide synthase (NOS) isoforms: neuronal (nNOS), inducible (iNOS), and endothelial (eNOS) all of which are found in the lung. While there are no isoform-specific inhibitors of NOS, the recent development and characterization of mice deficient in each of the NOS isoforms has allowed for more comprehensive study of the importance of NO in the lung circulation. Studies in the mouse have identified the role of NO from eNOS in modulating pulmonary vascular tone and in attenuating the development of chronic hypoxic pulmonary hypertension., K. A. Fagan, I. McMurtry, D. M. Rodman., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
1193. Nitric Oxide Synthase Inhibition and Glutamate Binding in Quinolinate-Lesioned Rat Hippocampus
- Creator:
- Václav Lisý and František Šťastný
- Format:
- print, bez média, and svazek
- Type:
- article, studie, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, fyziologie člověka, human physiology, Quinolinic acid, NMDA receptor, Membrane binding, Nitric oxide synthase (NOS), Neurodegeneration, 14, and 612
- Language:
- English
- Description:
- a1_The effect of lesions induced by bilateral intracerebroventricular (ICV) injection of quinolinate (250 nmol of QUIN/ventricle), a selective N-methyl-D-aspartate (NMDA) receptor agonist, on [3H]glutamate ([3H]Glu) binding to the main types of both ionotropic and metabotropic glutamate receptors (iGluR and mGluR) was investigated in synaptic membrane preparations from the hippocampi of 50-day-old rats. The membranes from QUIN injured brains revealed significantly lowered binding in iGluR (by 31 %) as well as in mGluR (by 22 %) as compared to the controls. Using selected glutamate receptor agonists as displacers of [3H]Glu binding we found that both the NMDA-subtype of iGluR and group I of mGluR are involved in this decrease of binding. Suppression of nitric oxide (NO) production by NG-nitro-L-arginine (50 nmol of NARG/ventricle) or the increase of NO generation by 3-morpholinylsydnoneimine (5 nmol of SIN-1/ventricle) failed to alter [3H]Glu or [3H]CPP (3-((D)-2-carboxypiperazin-4-yl)-[1,2-3H]-propyl-1-phosphonic acid; NMDA-antagonist) binding declines caused by QUIN-lesions. Thus, our findings indicate that both the NMDA-subtype of iGluR and group I of mGluR are susceptible to the QUIN-induced neurodegeneration in the rat hippocampus. However, the inhibition of NO synthesis did not reveal any protective action in the QUIN-evoked, NMDA-receptor mediated decrease of [3H]Glu binding., a2_Therefore, the additional mechanisms of QUIN action, different from direct NMDA receptor activation/NO production (e.g. lipid peroxidation induced by QUIN-Fe-complexes) cannot be excluded., V. Lisý, F. Šťastný., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
1194. Nitric oxide synthase mRNA levels correlate with gene expression of angiotensin II type-1 but not type-2 receptors, renin or angiotensin converting enzyme in selected brain areas
- Creator:
- Křižanová, O., Kiss, A., Žáčiková, Ľ., and Daniela Ježová
- Format:
- print, bez média, and svazek
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, genová exprese, mozek, gene expression, brain, angiotensin II, nitric oxide synthase, AT1 receptors, AT2 receptors, rat brain, 14, and 612
- Language:
- English
- Description:
- Recent data suggest that there is interaction between peripheral angiotensin II and nitric oxide. However, sparse information is available on the mutual interaction of these two compounds in the brain. The potential intercourse of nitric oxide with brain neuropeptides needs to be substantiated by assessing its local production and gene expression of the synthesizing enzymes involved. The aim of the present study was to evaluate whether the gene expression of brain nitric oxide synthase (bNOS) is related to the sites of gene expression of different components of the rat brain renin angiotensin system (renin, angiotensin converting enzyme (ACE) or angiotensin receptors of AT1 and AT2 subtypes). The levels of corresponding mRNAs were measured and correlated in nine structures of adult rat brain (hippocampus, amygdala, septum, thalamus, hypothalamus, cortex, pons, medulla and cerebellum). As was expected, positive correlation was observed between renin and angiotensin-converting enzyme mRNAs. Moreover, a significant correlation was found between brain NO synthase and AT1 receptor mRNAs, but not with mRNA of the AT2 receptor, ACE and renin. Parallel distribution of mRNAs coding for bNOS and AT1 receptors in several rat brain structures suggests a possible interaction between brain angiotensin II and nitric oxide, which remains to be definitely demonstrated by other approaches., O. Križanová, A. Kiss, Ľ. Žáčiková, D. Ježová., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
1195. Nitric oxide-compromised hypertension: facts and enigmas
- Creator:
- Mária Gerová
- Format:
- print, bez média, and svazek
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, hypertenze, polyaminy, hypertension, polyamines, 14, and 612
- Language:
- English
- Description:
- NO concentration in the femoral artery and femoral vein of anesthetized dogs was found to be 154.2± 5.6 nM and 90.0± 12 nM, respectively. Inhibition of NO synthase (NOS) slightly decreased the basal NO concentration in femoral artery from 154.2± 5.6 to 137.2± 3.3 nM. Acetylcholine-induced increase in NO concentration was slightly but still significantly attenuated, suggesting that very probably L-NAME did not inhibit all sources of nitric oxide (NO). Local NOS inhibition in the posterior hypothalamus dose-dependently increased systemic blood pressure (BP) in rats. Short-term general NOS inhibition in anesthetized dogs increased diastolic BP but not systolic BP. The heart rate after one-hour down-fluctuation returned to initial values. Proteosynthesis in the myocardium and both branches of the left coronary artery increased, but this was not supported by polyamines, since the activity of ornithine decarboxylase declined. Long-term general NOS inhibition elicited a sustained BP increase, a decrease in heart rate, cardiac hypertrophy and an increase in wall thickness of the coronary and carotid artery. The results indicate that NO deficiency itself plays a role in proteosynthesis and cardiac hypertrophy, in spite of relatively small increase in diastolic blood pressure and no change in systolic blood pressure, at least after an acute L-NAME administration. The hypotension response to acetylcholine and bradykinin studied in anesthetized NO-compromised rats, was unexpectedly enhanced. The elucidation of this paradoxical phenomenon will require further experiments., M. Gerová., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
1196. Nitrotyrosine and nitrate/nitrite levels in cardiac arrest survivors treated with endovascular hypothermia
- Creator:
- Krüger, A., Petr Ošťádal, Vondráková, D., Janotka, M., and Jan Herget
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, fyziologie člověka, human physiology, cardiac arrest, hypothermia, nitrotyrosine, nitrates/nitrites, oxidative stress, 14, and 612
- Language:
- English
- Description:
- The protective effect of therapeutic hypothermia in cardiac arrest survivors (CAS) has been previously well documented. Animal studies have indicated that attenuation of tissue oxidative stress (OS) may be involved in the mechanisms that lead to the beneficial effect of hypothermia. The extent of OS and nitric oxide (NO) production in adult CAS treated with endovascular hypothermia is, however, unknown. A total of 11 adult patients who experienced cardiac arrest out of hospital were included in the present study, and all were treated with mild hypothermia using the Thermogard XP (Alsius, USA) endovascular system. A target core temperature of 33 °C was maintained for 24 hours, with a subsequent rewarming rate of 0.15 °C per hour, followed by normothermia at 36.8 °C. Blood samples for the measurement of nitrotyrosine and nitrate/nitrite levels were drawn at admission and every 6 hours thereafter for two days. During the hypothermic period, the levels of nitrotyrosine and nitrates/nitrites were comparable with baseline values. During the rewarming period, serum levels of both parameters gradually increased and, during the normothermic period, the levels were significantly higher compared with hypothermic levels (nitrotyrosine, P<0.001; nitrates/nitrites, P<0.05). In our study, significantly lower levels of nitrotyrosine and nitrates/nitrites were demonstrated during hypothermia compared with levels during the normothermic period in adult CAS. These data suggest that attenuation of OS and NO production may be involved in the protective effect of hypothermia in adult CAS., A. Krüger ... [et al.]., and Obsahuje seznam literatury
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
1197. NMDA and AMPA receptors: development and status epilepticus
- Creator:
- Szczurowska, E. and Pavel Mareš
- Format:
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, mozek, mutace (biologie), epilepsie, brain, mutation (biology), epilepsy, glutamate receptors, 14, and 612
- Language:
- English
- Description:
- Glutamate is the main excitatory neurotransmitter in the brain and ionotropic glutamate receptors mediate the majority of excitatory neurotransmission (Dingeldine et al. 1999). The high level of glutamatergic excitation allows the neonatal brain (the 2 nd postnatal week in rat) to develop quickly but it also makes it highly prone to age-specific seizures that can cause lifelong neurological and cognit ive disability (Haut et al. 2004). There are three types of ionotropic glutamate receptors (ligand-gated ion channels) named according to their prototypic agonists: N- methyl-D-aspartate (NMDA), 2-amino-3-(3-hydroxy-5-methyl-isoxazol-4-yl) propanoic acid (AMPA) and kainate (KA). During early stages of postnatal development glutamate receptors of NMDA and AMPA type undergo intensive functional changes owing to modifications in their subunit composition (Carter et al. 1988, Watanabe et al. 1992, Monyer et al. 1994, Wenzel et al. 1997, Sun et al. 1998, Lilliu et al. 2001, Kumar et al. 2002, Matsuda et al. 2002, Wee et al. 2008, Henson et al. 2010, Pachernegg et al. 2012, Paoletti et al. 2013). Participation and role of these receptors in mechanisms of seizures and epilepsy became one of the main targets of intensive investigation (De Sarro et al. 2005, Di Maio et al. 2012, Rektor 2013). LiCl/Pilocarpine (LiCl/Pilo) induced status epilepticus is a model of severe seizures resulting in development temporal lobe epilepsy (TLE). This review will consider developmental changes and contribution of NMDA and AMPA receptors in LiCl/Pilo model of status epilepticus in immature rats., E. Szczurowska, P. Mareš., and Obsahuje bibliografii a bibliografické odkazy
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
1198. NMR plasma metabolomics study of patients overcoming acute myocardial infarction: in the first 12 h after onset of chest pain with statistical discrimination towards metabolomic biomarkers
- Creator:
- Petráš, Martin, Sarlinova, Miroslava, Kalenska, Dagmar, Samoš, Matej, Bolek, Tomáš, Racay, Peter, Halašová, Erika, Štrbák, Oliver, Staško, Ján, Musak, Ludovit, Skorvanova, Michaela, and Baranovicova, Eva
- Format:
- počítač and online zdroj
- Type:
- model:article and TEXT
- Subject:
- infarkt myokardu, myocardial infarction, plasma, NMR metabolomics, 14, and 612
- Language:
- English
- Description:
- Acute myocardial infarction (AMI) is one of the leading causes of death among adults in older age. Understanding mechanisms how organism responds to ischemia is essential for the ischemic patient’s prevention and treatment. Despite the great prevalence and incidence only a small number of studies utilize a metabolomic approach to describe AMI condition. Recent studies have shown the impact of metabolites on epigenetic changes, in these studies plasma metabolites were related to neurological outcome of the patients making metabolomic studies increasingly interesting. The aim of this study was to describe metabolomic response of an organism to ischemic stress through the changes in energetic metabolites and aminoacids in blood plasma in patients overcoming acute myocardial infarction. Blood plasma from patients in the first 12 h after onset of chest pain was collected and compared with volunteers without any history of ischemic diseases via NMR spectroscopy. Lowered plasma levels of pyruvate, alanine, glutamine and neurotransmitter precursors tyrosine and tryptophan were found. Further, we observed increased plasma levels of 3-hydroxybutyrate and acetoacetate in balance with decreased level of lipoproteins fraction, suggesting the ongoing ketonic state of an organism. Discriminatory analysis showed very promising performance where compounds: lipoproteins, alanine, pyruvate, glutamine, tryptophan and 3-hydroxybutyrate were of the highest discriminatory power with feasibility of successful statistical discrimination., Martin Petras, Dagmar Kalenska, Matej Samos, Tomas Bolek, Miroslava Sarlinova, Peter Racay, Erika Halasova, Oliver Štrbák, Jan Stasko, Ludovit Musak, Michaela Skorvanova, Eva Baranovicova., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/publicdomain/mark/1.0/ and policy:public
1199. Nodose ganglia-modulatory effects on respiration
- Creator:
- Kaczyńska, K. and Szereda-Przestaszewska, M
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, fyziologie člověka, human physiology, vagus nerve, nodose ganglion, respiratory pattern, apnoea, neurotransmitters, 14, and 612
- Language:
- English
- Description:
- The key role of the vagus nerves in the reflex control of breathing is generally accepted. Cardiopulmonary vagal receptors and their afferent connection with the medullary respiratory centers secures the proper regulatory feedback. Section of the vagi at the midcervical level interrupts primary vagal reflexes and those due to activation of lung afferents by neuroactive substances. In this context the present review focuses on the reflex contribution of the inferior (nodose) vagal ganglia to the respiratory pattern, considering that this structure contains perikarya of vagal afferent neurons which house neurotransmitters, neuropeptides and neurochemical substances. In experimental animals with removed sensory input from the lungs (midcervical vagotomy) the following evidence was reported. Transient respiratory suppression in the form of apnoea, occuring after systemic injection of serotonin, adenosine triphosphate and anandamide (N-arachidonoyl-ethanolamine-endogenous cannabinoid neurotransmitter), which was abrogated by nodose ganglionectomy. Preserved nodose-NTS connection conditioned respiratory depression affecting the timing component of the breathing pattern evoked by N-6-cyclopentyl-adenosine (CPA) and inhibition of both respiratory constituents induced by NPY. Stimulatory effect of NPY13-36 on tidal volume required nodosal connection. The cardiovascular effects of majority of the tested substances occurred beyond the nodose ganglia (with exclusion of serotonin and anandamide)., K. Kaczyńska, M. Szereda-Przestaszewska., and Obsahuje seznam literatury
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
1200. Non-quantal acetylcholine release at the neuromuscular junction
- Creator:
- František Vyskočil, Malomouzh, A. I., and Nikolsky, E. E.
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, fyziologie, acetylcholin, synapse, oxid dusnatý, hibernace, physiology, acetylcholine, synapses, nitric oxide, hibernation, non-quantal release, neuromuscular junction, desensitization, resting membrane potential, choline transporter, vesicular ACh transporter, anticholinesterase, N-acetylaspartylglutamate, miniature endplate potential, 14, and 612
- Language:
- English
- Description:
- There are two principal mechanisms of acetylcholine (ACh) release from the resting motor nerve terminal: quantal and non-quantal (NQR); the former being only a small fraction of the total, at least at rest. In the present article we summarize basic research about the NQR that is undoubtedly an important trophic factor during endplate development and in adult neuromuscular contacts. NQR helps to eliminate the polyneural innervation of developing muscle fibers, ensures higher excitability of the adult subsynaptic membrane by surplus polarization and protects the RMP from depolarization by regulating the NO cascade and chloride transport. It shortens the endplate potentials by promoting postsynaptic receptor desensitization when AChE is inhibited during anti-AChE poisoning. In adult synapses, it can also activate the electrogenic Na+/K+-pump, change the degree of synchronization of quanta released by the nerve stimulation and affects the contractility of skeletal muscles., F. Vyskočil, A. I. Malomouzh, E. E. Nikolsky., and Obsahuje seznam literatury
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public