Number of results to display per page
Search Results
252. Microinjection of salusin-β into the nucleus tractus solitarii inhibits cardiovascular function by suppressing presympathetic neurons in rostral ventrolateral medulla in rats
- Creator:
- Lu, Y., Wu, Y. S., Chen, D. S., Wang, M. M., Wang, W. Z., and Yuan, W. J.
- Format:
- print, bez média, and svazek
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, fyziologie, neurony, physiology, neurons, salusin, medulla, baroreflex, presympathetic neuron, rat, 14, and 612
- Language:
- English
- Description:
- Salusin-β is newly identified bioactive peptide of 20 amino acids, which is widely distributed in hematopoietic system, endocrine system, and the central nervous system (CNS). Although salusin- β extensively expressed in the CNS, the central cardiovascular functions of salusin-β are unclear. Our main objective was to determine the cardiovascular effect of microinjection of salusin-β into the nucleus tractus solitarii (NTS) in anesthetized rats. Bilateral or unilateral microinjection of salusin-β (0.94-94 μg/rat) into the NTS dose-dependently decreased blood pressure and heart rate. Bilateral NTS microinjection of salusin-β (9.4 μg/rat) did not alter baroreflex sensitivity. Prior application of the glutamate receptor antagonist kynurenic acid (0.19 μg/rat, n=9) into the NTS did not alter the salusin-β (9.4 μg/rat) induced hypotension and bradycardia. However, pretreatment with the GABA receptor agonist muscimol (0.5 ng/rat) within the rostral ventrolateral medulla (RVLM) completely abolished the hypotension (-14±5 vs. -3±5 mm Hg, P <0.05) and bradycardia (-22±6 vs. -6±5 bpm, P <0.05) evoked by intra-NTS salusin-β (9.4 μg/rat). In addition, we found that vagotomy didn’t influence the actions of salusin-β (9.4 μg/rat) in the NTS. In conclusion, our present study shows that microinjection of salusin-β into the NTS significantly produces hypotension and bradycardia, presumably by suppressing the activities of presympathetic neurons in the RVLM., Y. Lu, Y. S. Wu, D. S. Chen, M. M. Wang, W. Z. Wang, W. J. Yuan., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
253. Microvascular endothelial cells from human omentum lack an inward rectifier K+ current
- Creator:
- Himmel, H. M., Rauen, U., and Ravens, U.
- Format:
- print, bez média, and svazek
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, fyziologie, physiology, whole-cell voltage clamp, ion substitution, non-excitable cells, Na+ background current, chloride conductance, CA 2+ - activated K+ current, 14, and 612
- Language:
- English
- Description:
- In most macrovascular endothelial cell (EC) preparations, resting membrane potential is determined by the inwardly rectifying K+ current (IK1), whereas in microvascular EC the presence of IK1 varies markedly. Cultured microvascular EC from small vessels of human omentum were examined by means of the voltage-clamp technique to elucidate the putative role of IK1 in maintaining resting membrane potential. Macrovascular EC from human iliac artery and bovine aorta served as reference. Human omentum EC showed an outwardly rectifying current-voltage relation. Inward current was hardly sensitive to variations of extracellular [K+] and Ba2+ block suggesting lack of IK1. However, substitution of extracellular [Na+] and/or [Cl-] affected the current-voltage relation indicating that Na+ and Cl- contribute to basal current. Furthermore, outward current was reduced by tetraethylammonium (10 mM), and cell-attached recordings suggested the presence of a Ca2+-activated K+ current. In contrast to human omentum EC, EC from human iliac artery and bovine aorta possessed inwardly rectifying currents which were sensitive to variations of extracellular [K+] and blocked by Ba2+. Thus, the lack of IK1 in human omentum EC suggests that resting membrane potential is determined by Na+ and Cl- currents in addition to K+ outward currents., H. M. Himmel, U. Rauen, U. Ravens., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
254. Moderate exercise based on artificial gravity preserves orthostatic tolerance and exercise capacity during short-term head-down bed rest
- Creator:
- Li, X.-T., Yang, C.-B., Zhu, Y.-S., Sun, J., Shi, F., Wang, Y.-C., Gao, Y., Zhao, J.-D., and Sun, X.-Q.
- Format:
- print, bez média, and svazek
- Type:
- article, články, journal articles, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, fyziologie, physiology, short arm centrifuge, microgravity, maximal oxygen consumption, anaerobic threshold, cardiovascular function, heart rate variability, 14, and 612
- Language:
- English
- Description:
- Numerous countermeasures have been proposed to minimize microgravity-induced physical deconditioning, but their benefits are limited. The present study aimed to investigate whether personalized aerobic exercise based on artificial gravity (AG) mitigates multisystem physical deconditioning. Fourteen men were assigned to the control group (n=6) and the countermeasure group (CM, n=8). Subjects in the CM group were exposed to AG (2 Gz at foot level) for 30 min twice daily, during which time cycling exercise of 80-95 % anaerobic threshold (AT) intensity was undertaken. Orthostatic tolerance (OT), exercise tests, and blood assays were determined before and after 4 days head-down bed rest (HDBR). Cardiac systolic function was measured every day. After HDBR, OT decreased to 50.9 % and 77.5 % of pre-HDBR values in control and CM groups, respectively. Exercise endurance, maximal oxygen consumption, and AT decreased to 96.5 %, 91.5 % and 91.8 % of pre-HDBR values, respectively, in the control group. Nevertheless, there were slight changes in the CM group. HDBR increased heart rate, sympathetic activity, and the pre-ejection period, but decreased plasma volume, parasympathetic activity and left-ventricular ejection time in the control group, whereas these effects were eliminated in the CM group. Aldosterone had no change in the control group but increased significantly in the CM group. Our study shows that 80-95 % AT aerobic exercise based on 2 Gz of AG preserves OT and exercise endurance, and affects body fluid regulation during short-term HDBR. The underlying mechanisms might involve maintained cardiac systolic function, preserved plasma volume, and improved sympathetic responses to orthostatic stress., X.-T. Li, C.-B. Yang, Y.-S. Zhu, J. Sun, F. Shi, Y.-C. Wang, Y. Gao, J.-D. Zhao, X.-Q. Sun., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/publicdomain/mark/1.0/ and policy:public
255. Modulation of antioxidant enzyme activities by sexual steroid hormones
- Creator:
- Snežana B. Pajović and Saičić, Z. S.
- Format:
- print, bez média, and svazek
- Type:
- article, články, model:article, and TEXT
- Subject:
- Experimentální medicína, fyziologie, potkan, physiology, Rattus norvegicus, brain, antioxidant defense enzymes, sexual steroid hormones, 14, and 616-092
- Language:
- English
- Description:
- Taking into consideration the biological importance of interaction between antioxidant defense (AD) enzymes and sexual steroid hormones it was deemed important to compare our recent achievements in the field with the state of current knowledge. The main goal of the present review was to investigate the changes of AD enzyme activities: superoxide dismutases, catalase, glutathione peroxidase, glutathione-S-transferase and glutathione reductase in the brain of female and male rats depending on progesterone and estradiol. These ovarian steroids produce their effects by acting on numerous target tissues and organs, such as the reproductive organs, bone tissue and cartilage, peripheral blood vessels and the central nervous system (CNS). We have chosen it as a new parameter that might represent an important indicator of the changes within the CNS, bearing in mind the biological importance of the enzymes of the AD system. Our experimental results indicate that the AD enzyme activities in the brain tissue of female and male rats show a certain dependence on the concentration of progesterone and estradiol. The present review suggests that the modulation of the oxidative and antioxidative capacity by sexual steroid hormones is mediated through antioxidant metabolizing enzymes., S. B. Pajović, Z. S. Saičić., and Obsahuje bibliografii a bibliografické odkazy
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
256. Modulation of substance P signaling by dipeptidyl peptidase-IV enzymatic activity in human glioma cell lines
- Creator:
- Petr Bušek, Jarmila Stremeňová, Evžen Křepela, and Aleksi Šedo
- Format:
- print, bez média, and svazek
- Type:
- article, články, model:article, and TEXT
- Subject:
- Biochemie. Molekulární biologie. Biofyzika, fyziologie, gliomy, vápník, physiology, gliomas, calcium, dipeptidyl peptidase, substance P, NK1 receptor, calcium signaling, 2, and 577
- Language:
- English
- Description:
- Dipeptidyl peptidase-IV (DPP-IV, CD26) is a serine protease almost ubiquitously expressed on cell surface and present in body fluids. DPP-IV has been suggested to proteolytically modify a number of biologically active peptides including substance P (SP) and the chemokine stro mal cell derived factor-1α (SDF-1α, CXCL12). SP and SDF-1α have been implicated in the regulation of multiple biological processes and also induce responses that may be relevant for glioma progression. Both SP and SDF-1α are signaling through cell surface receptors and use intracellular calcium as a second messenger. The effect of DPP-IV on intracellular calcium mobilization mediated by SP and SDF- α was monitored in suspension of wild type U373 and DPP-IV transfected U373DPPIV glioma cells using indicator FURA-2. Nanomolar concentrations of SP triggered a transient dose dependent increase in intracellular calcium rendering the cells refractory to repeated stimulation, while SDF-1α had no measurable effect. SP signaling in DPP-IV overexpressing U373DPPIV cells was not substantially different from that in wild type cells. However, preincubation of SP with the DPP-IV overexpressing cells lead to the loss of its signaling potential, which could be prevented with DPP-IV inhibitors. Taken together, DPP-IV may proteolytically inactivate local mediators involved in gliomagenesis., P. Bušek, J, Stremeňová, E. Křepela, A. Šedo., and Obsahuje bibliografii a bibliografické odkazy
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
257. Molecular basis of TRPA1 regulation in nociceptive neurons: a review
- Creator:
- Kádková, A., Synytsya, V., Krusek, J., Zímová, L., and Vlachová, V.
- Format:
- print, bez média, and svazek
- Type:
- article, články, journal articles, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, fyziologie, physiology, transient receptor potential ankyrin 1, bradykinin, structure - function, nociception, post-translational modifications, signaling pathways, 14, and 612
- Language:
- English
- Description:
- Transient receptor potential A1 (TRPA1) is an excitatory ion channel that functions as a cellular sensor, detecting a wide range of proalgesic agents such as environmental irritants an d endogenous products of inflammation and oxidative stress. Topical application of TRPA1 agonists produces an acute nociceptive response through peripheral release of neuropeptides, purines and other transmitters from activated sensory nerve endings. This, in turn, further regulates TRPA1 activity downstream of G-protein and phospholipase C -coupled signaling cascades. Despite the important physiological relevance of such regulation leading to nociceptor sensitization and consequent pain hypersensitivity, th e specific domains through which TRPA1 undergoes post -translational modifications that affect its activation properties are yet to be determined at a molecular level. This review aims at providing an account of our current knowledge on molecular basis of r egulation by neuronal inflammatory signaling pathways that converge on the TRPA1 channel protein and through modification of its specific residues influence the extent to which this channel may contribute to pain., A. Kádková, V. Synytsya, J. Krusek, L. Zímová, V. Vlachová., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/publicdomain/mark/1.0/ and policy:public
258. Monocolonization with Bacteroides ovatus protects immunodeficient SCID mice from mortality in chronic intestinal inflammation caused by long-lasting dextran sodium sulfate treatment
- Creator:
- Hudcovic, T., Hana Kozáková, Jiřina Kolínská, Štěpánková, R., Hrnčíř, T., and Helena Tlaskalová
- Format:
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, fyziologie, ulcerózní kolitida, myši, physiology, ulcerative colitis, mice, Bacteroides ovatus, dextran sulfate sodium colitis, gnotobiotic mice, 14, and 612
- Language:
- English
- Description:
- This study was aimed to evaluate the role of commensal Gram-negative bacterium Bacteroides ovatus in murine model of chronic intestinal inflammation. The attempt to induce chronic colitis was done in Bacteroides ovatus-monoassociated, germ-free and conventional mice either in immunocompetent (BALB/c) mice or in mice with severe combined immunodeficiency (SCID), using 2.5 % dextran-sodium sulfate (DSS) in drinking water (7 days DSS, 7 days water, 7 days DSS). Conventional mice developed chronic colitis. Some of germ-free BALB/c and the majority of germ-free SCID mice did not survive the long-term treatment with DSS due to massive bleeding into the intestinal lumen. However, monocolonization of germ-free mice of both strains with Bacteroides ovatus prior to long-term treatment with DSS protected mice from bleeding, development of intestinal inflammation and precocious death. We observed that though DSS-treated Bacteroides ovatus-colonized SCID mice showed minor morphological changes in colon tissue, jejunal brush-border enzyme activities such as γ-glutamyltranspeptidase, lactase and alkaline phosphatase were significantly reduced in comparison with DSS-untreated Bacteroides ovatus-colonized mice. This modulation of the enterocyte γ-glutamyltranspeptidase localized to the brush border membrane has been described for the first time. This enzyme is known to reflect an imbalance between pro-oxidant and anti-oxidant mechanisms, which could be involved in protective effects of colonization of germ-free mice with Bacteroides ovatus against DSS injury., T. Hudcovic ... [et al.]., and Obsahuje seznam literatury
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
259. Mutation analysis of candidate genes SCN1B, KCND3 and ANK2 in patients with clinical diagnosis of long QT syndrome
- Creator:
- Martina Raudenská, Alexandra Bittnerová, Tomáš Novotný, Alena Floriánová, Karel Chroust, Renata Gaillyová, Bořivoj Semrád, Jitka Kadlecová, Martina Šišáková, Ondřej Toman, and Jindřich Špinar
- Format:
- print, bez média, and svazek
- Type:
- article, články, model:article, and TEXT
- Subject:
- Biochemie. Molekulární biologie. Biofyzika, fyziologie, genetika, geny, physiology, genetics, genes, ANK2, candidate geens, KCND3, long QT syndrome, SCN1B, 2, and 577
- Language:
- English
- Description:
- The long QT syndrome (LQTS) is a monogenic disorder characterized by prolongation of the QT interval on electrocardiogram and syncope or sudden death caused by polymorphic ventricular tachycardia (torsades de pointes). In general, mutations in cardiac ion channel genes (KCNQ1, KCNH2, SCN5A, KCNE1, KCNE2) have been identified as a cause for LQTS. About 50-60 % of LQTS patients have an identifiable LQTS causing mutation in one of mentioned genes. In a group of 12 LQTS patients with no identified mutations in these genes we have tested a hypothesis that other candidate genes could be involved in LQTS pathophysiology. SCN1B and KCND3 genes encode ion channel proteins, ANK2 gene encodes cytoskeletal protein interacting with ion channels. To screen coding regions of genes SCN1B, KCND3, and 10 exons of ANK2 following methods were used: PCR, SSCP, and DNA sequencing. Five polymorphisms were found in screened candid ate genes, 2 polymorphisms in KCND3 and 3 in SCN1B. None of found polymorphisms has coding effect nor is located close to splice sites or has any similarity to known splicing enhancer motifs. Polymorphism G246T in SCN1B is a novel one. No mutation directly causing LQTS was found. Molecular mechanism of LQTS genesis in these patients remains unclear., M. Raudenská, A. Bittnerová, T. Novotný, A. Floriánová, K. Chroust, R. Gaillyová, B. Semrád, J. Kadlecová, M. Šišáková, O. Toman, J. Špinar., and Obsahuje bibliografii a bibliografické odkazy
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
260. Myocardial phospholipid remodeling under different types of load imposed during early postnatal development
- Creator:
- František Novák, František Kolář, Blanka Hamplová, Mrnka, L., Václav Pelouch, Bohuslav Ošťádal, and Olga Nováková
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, fyziologie, myokard, poporodní péče, physiology, myocardium, postnatal care, phospholipids, cardiolipin, pressure overload, chronic hypoxia, thyroid status, 14, and 612
- Language:
- English
- Description:
- Normal increase in hemodynamic load during early postnatal life is associated with heart growth and maturation of membrane structures that is accompanied by remodeling of membrane protein and lipid components. This review describes remodeling of phospholipids (PL) in rat myocardium during normal postnatal development and during accelerated cardiac growth induced by additional workload (aorta constriction, chronic hypoxia and hyperthyroidism) imposed on the heart early after birth. Normal physiological load after birth stimulates the development of membrane structures and synthesis of PL. While hyperthyroidism accelerates these processes, pressure overload has an inhibitory effect. These changes primarily influence the maturation of mitochondrial membranes as cardiolipin is one of the most affected PL species. The most sensitive part of PL structure in their remodeling process are PL acyl chains, particularly polyunsaturated fatty acids that are the key components determining the basic physicochemical properties of the membrane bilayer and thus the function of membrane-bound proteins and membrane-derived signaling lipid molecules. It is evident that PL remodeling may significantly influence both normal and pathological postnatal development of myocardium., F. Novák ... [et al.]., and Obsahuje seznam literatury
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public