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Relevant bibliographies by topics / Cardiac receptors

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Academic literature on the topic 'Cardiac receptors'

Author: Grafiati

Published: 4 June 2021

Last updated: 20 February 2023

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Journal articles on the topic "Cardiac receptors"

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SAXENA, P. "Cardiac serotonin receptors." Journal of Molecular and Cellular Cardiology 18 (1986): 60. http://dx.doi.org/10.1016/s0022-2828(86)80659-9.

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Yang, Ronghua, and Bruce T. Liang. "Cardiac P2X 4 Receptors." Circulation Research 111, no. 4 (August 3, 2012): 397–401. http://dx.doi.org/10.1161/circresaha.112.265959.

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ANGUS, J. "Cardiac receptors — An overview." Journal of Molecular and Cellular Cardiology 18 (1986): 1. http://dx.doi.org/10.1016/s0022-2828(86)80491-6.

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Boivin-Jahns, V., A. Schlipp, S. Hartmann, P. Panjwani, K. Klingel, M. J. Lohse, G. Ertl, and R. Jahns. "Antibodies to cardiac receptors." Herz 37, no. 8 (November 28, 2012): 843–48. http://dx.doi.org/10.1007/s00059-012-3699-5.

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Woo, Sun-Hee, and Tran Nguyet Trinh. "P2 Receptors in Cardiac Myocyte Pathophysiology and Mechanotransduction." International Journal of Molecular Sciences 22, no. 1 (December 29, 2020): 251. http://dx.doi.org/10.3390/ijms22010251.

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ATP is a major energy source in the mammalian cells, but it is an extracellular chemical messenger acting on P2 purinergic receptors. A line of evidence has shown that ATP is released from many different types of cells including neurons, endothelial cells, and muscle cells. In this review, we described the distribution of P2 receptor subtypes in the cardiac cells and their physiological and pathological roles in the heart. So far, the effects of external application of ATP or its analogues, and those of UTP on cardiac contractility and rhythm have been reported. In addition, specific genetic alterations and pharmacological agonists and antagonists have been adopted to discover specific roles of P2 receptor subtypes including P2X4-, P2X7-, P2Y2- and P2Y6-receptors in cardiac cells under physiological and pathological conditions. Accumulated data suggest that P2X4 receptors may play a beneficial role in cardiac muscle function, and that P2Y2- and P2Y6-receptors can induce cardiac fibrosis. Recent evidence further demonstrates P2Y1 receptor and P2X4 receptor as important mechanical signaling molecules to alter membrane potential and Ca2+ signaling in atrial myocytes and their uneven expression profile between right and left atrium.

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Li, De-Pei, David B. Averill, and Hui-Lin Pan. "Differential roles for glutamate receptor subtypes within commissural NTS in cardiac-sympathetic reflex." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 281, no. 3 (September 1, 2001): R935—R943. http://dx.doi.org/10.1152/ajpregu.2001.281.3.r935.

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Ischemic stimulation of cardiac receptors evokes excitatory sympathetic reflexes. Although the nucleus of the solitary tract (NTS) is an important site for integration of visceral afferents, its involvement in the cardiac-renal sympathetic reflex remains to be fully defined. This study examined the role of glutamate receptor subtypes in the commissural NTS in the sympathetic responses to stimulation of cardiac receptors. Renal sympathetic nerve activity (RSNA) was recorded in anesthetized rats. Cardiac receptors were stimulated by epicardial application of bradykinin (BK; 10 μg/ml). Application of BK significantly increased the mean arterial pressure from 78.2 ± 2.2 to 97.5 ± 2.9 mmHg and augmented RSNA by 38.5 ± 2.5% ( P < 0.05). Bilateral microinjection of 10 pmol of 6-cyano-7-nitroquinoxaline-2,3-dione, a non- N-methyl-d-aspartate (NMDA) antagonist, into the commissural NTS eliminated the pressor and RSNA responses to BK application in 10 rats. However, microinjection of 2-amino-5-phosphonopentanoic acid (0.1 and 1 nmol, n = 8), an NMDA- receptor antagonist, or α-methyl-4-carboxyphenylglycine (0.1 and 1 nmol, n = 5), a glutamate metabotropic receptor antagonist, failed to attenuate significantly the pressor and RSNA responses to stimulation of cardiac receptors with BK. Thus this study suggests that non-NMDA, but not NMDA and glutamate metabotropic, receptors in the commissural NTS play an important role in the sympathoexcitatory reflex response to activation of cardiac receptors during myocardial ischemia.

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Smith, William H. T., R. Unnikrishnan Nair, Dawn Adamson, Mark T. Kearney, Stephen G. Ball, and Anthony J. Balmforth. "Somatostatin receptor subtype expression in the human heart: differential expression by myocytes and fibroblasts." Journal of Endocrinology 187, no. 3 (December 2005): 379–86. http://dx.doi.org/10.1677/joe.1.06082.

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In acromegaly, somatostatin receptor ligands (SRLs) can ameliorate left ventricular hypertrophy (LVH) and their use is associated with demonstrable improvements in various parameters of cardiac function. It remains unclear as to whether these beneficial effects are principally attributable to falling GH and IGF-I levels, or whether SRLs exert independent direct effects on the heart via somatostatin receptors. To help address this issue, we have sought to investigate somatostatin receptor expression in human heart. A human heart cDNA library was probed using PCR techniques to determine expression of somatostatin receptor subtypes. Subsequently, human heart biopsies and human cardiac fibroblasts and myocytes were analysed to determine whether expression differed between cardiac chambers or cell types. mRNAs for four of the five somatostatin receptor subtypes (sst1, sst2, sst4 and sst5) were shown to be co-expressed by the human heart. These receptors were present in both atrial and ventricular tissue. Human cardiac myocytes expressed mRNA for only sst1 and sst2, while human cardiac fibroblasts expressed all four subtypes found in whole heart tissue. The expression of functional somatostatin receptors on human cardiac fibroblasts was confirmed by mobilisation of intracellular calcium in response to somatostatin. The presence of cardiac somatostatin receptors raises the possibility of a direct effect of somatostatin analogues on the heart. Furthermore, the differential expression of somatostatin receptor subtypes by human cardiac myocytes and fibroblasts opens up the possibility of differential modulation of the cell types in the heart by subtype-specific somatostatin analogues.

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Sagawa, Toshio, Kazuko Sagawa, James E. Kelly, Robert G. Tsushima, and J. Andrew Wasserstrom. "Activation of cardiac ryanodine receptors by cardiac glycosides." American Journal of Physiology-Heart and Circulatory Physiology 282, no. 3 (March 1, 2002): H1118—H1126. http://dx.doi.org/10.1152/ajpheart.00700.2001.

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This study investigated the effects of cardiac glycosides on single-channel activity of the cardiac sarcoplasmic reticulum (SR) Ca2+ release channels or ryanodine receptor (RyR2) channels and how this action might contribute to their inotropic and/or toxic actions. Heavy SR vesicles isolated from canine left ventricle were fused with artificial planar lipid bilayers to measure single RyR2 channel activity. Digoxin and actodigin increased single-channel activity at low concentrations normally associated with therapeutic plasma levels, yielding a 50% of maximal effect of ∼0.2 nM for each agent. Channel activation by glycosides did not require MgATP and occurred only when digoxin was applied to the cytoplasmic side of the channel. Similar results were obtained in human RyR2 channels; however, neither the crude skeletal nor the purified cardiac channel was activated by glycosides. Channel activation was dependent on [Ca2+] on the luminal side of the bilayer with maximal stimulation occurring between 0.3 and 10 mM. Rat RyR2 channels were activated by digoxin only at 1 μM, consistent with the lower sensitivity to glycosides in rat heart. These results suggest a model in which RyR2 channel activation by digoxin occurs only when luminal [Ca2+] was increased above 300 μM (in the physiological range). Consequently, increasing SR load (by Na+ pump inhibition) serves to amplify SR release by promoting direct RyR2 channel activation via a luminal Ca2+-sensitive mechanism. This high-affinity effect of glycosides could contribute to increased SR Ca2+ release and might play a role in the inotropic and/or toxic actions of glycosides in vivo.

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Thompson, G. W., D. B. Hoover, J. L. Ardell, and J. A. Armour. "Canine intrinsic cardiac neurons involved in cardiac regulation possess NK1, NK2, and NK3 receptors." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 275, no. 5 (November 1, 1998): R1683—R1689. http://dx.doi.org/10.1152/ajpregu.1998.275.5.r1683.

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To determine whether intrinsic cardiac neurons involved in cardiac regulation possess neurokinin (NK) receptor subtypes, we administered selective NK receptor agonists individually (100 μM; 0.1 ml) into the coronary arterial blood supply of right atrial intrinsic cardiac neurons of 18 anesthetized dogs. The selective NK1 receptor agonist [Sar9,Met(O2)11]-substance P depressed the spontaneous activity of right atrial neurons (26.7 ± 6.7 to 13.0 ± 4.0 impulses/min; P < 0.05) in 11 dogs and augmented such activity in the other 5 dogs (8.0 ± 3.1 to 27.8 ± 8.7 impulses/min; P < 0.05). Local administration of the selective NK2 receptor agonist [β-Ala8]-NKA-(4—10) depressed right atrial neuronal activity (27.3 ± 6.4 to 14.7 ± 3.8 impulses/min; P < 0.05), whereas the selective NK3 receptor agonist senktide augmented such activity (18.9 ± 6.4 to 53.1 ± 12.0 impulses/min; P < 0.05). Left ventricular chamber pressure fell when selective NK1 and NK2 receptor agonists were administered. Increases in heart rate and right ventricular intramyocardial systolic pressure occurred when the selective NK3 receptor agonist was studied. Administration of a selective NK1or NK2 receptor antagonist altered neuronal activity, with no subsequent change in activity occurring after administration of its respective receptor agonist. Receptor autoradiography demonstrated tachykinin receptors associated with ventral right atrial intrinsic cardiac neurons. It is concluded that intrinsic cardiac neurons involved in cardiac regulation possess NK1, NK2, and NK3 receptors and that some intrinsic cardiac neurons receive tonic input via endogenously released NKs.

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Garcia, M. Iveth, and Darren Boehning. "Cardiac inositol 1,4,5-trisphosphate receptors." Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 1864, no. 6 (June 2017): 907–14. http://dx.doi.org/10.1016/j.bbamcr.2016.11.017.

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Dissertations / Theses on the topic "Cardiac receptors"

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Zhang, Weimin, and 張為民. "Cardiac k-opioid receptor: multiplicity, regulation, signal transduction and function." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1997. http://hub.hku.hk/bib/B3123804X.

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Sitsapesan, R. "Opioid receptors and ischaemia-induced cardiac arrhythmias." Thesis, University of Strathclyde, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.381536.

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Tai, Kwok-keung, and 戴國強. "A study on the cardiac k-opioid receptors: function, binding properties & signal transduction." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1993. http://hub.hku.hk/bib/B31233211.

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Tai, Kwok-keung. "A study on the cardiac k-opioid receptors : function, binding properties & signal transduction /." [Hong Kong] : University of Hong Kong, 1993. http://sunzi.lib.hku.hk/hkuto/record.jsp?B13441863.

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Asghari, Parisa. "Dynamic distribution of ryanodine receptors in cardiac muscles." Thesis, University of British Columbia, 2014. http://hdl.handle.net/2429/50492.

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The focus of this thesis is to address the location and distribution of the type 2 Ryanodine Receptor (RyR2) in mammalian cardiac myocytes with respect to their function. These integral membrane proteins function as Ca²⁺-activated Ca²⁺ ion channels as well as a scaffold for a large number of signaling molecules that modulate the release of Ca²⁺ through the channel. The relative position of the RyR2 tetramers is therefore a critical determinant of their function. To study this question, I have used a combination of immunofluorescence microscopy, transmission electron microscopy, and tomography to map the position of the tetramers in whole cells and in cell sections and have used tissue obtained from both rat and human hearts. Biochemical and physiological techniques were used to correlate structure with function. I have found that RyR2s are located only in three regions: in couplons on the surface, transverse tubules and on most of the axial tubules. In all regions, most but not all of the RyR2s colocalize with the voltage-gated Ca²⁺ channel (Cav1.2), suggesting that they play a role in excitation-contraction coupling. Some RyR2 are colocalized with cavelin-3 and not with Cav1.2 and hypothesized that these ‘extra-couplonic’ RyR2 might be regulated by the multitude of signaling molecules associated with caveolin-3 to modulate Ca²⁺ release. Dual-tilt electron tomography produced en face views of both rat and human dyads, enabling a direct examination of RyR2 arrangement. Both species showed that tetramer packing was non-uniform containing a mix of checkerboard and side-by-side arrangements as well as isolated tetramers. Finally, I showed that the tetramers’ arrangement depended on the Mg²⁺ concentration and on their phosphorylation status; in low Mg²⁺ and after phosphorylation RyR2s were positioned in largely checkerboard arrangements while in response to high Mg²⁺ the tetramers were positioned largely side by side. These tetramer arrangements: side by side, mixed and checkerboard were associated with progressively increasing spark frequencies. The correlation between tetramer arrangement and spark frequency suggests that tetramer rearrangement may be another mechanism whereby physiological processes operate and provides potential new mechanisms by which the activity of RYR2, the dyad and cardiac contractility may be regulated.
Medicine, Faculty of
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Crisp, Andrew John. "Cardiac ventricular receptors and the control of respiration." Thesis, University of Newcastle Upon Tyne, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.241355.

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Zhang, Weimin. "Cardiac k-opioid receptor : multiplicity, regulation, signal transduction and function /." Hong Kong : University of Hong Kong, 1997. http://sunzi.lib.hku.hk/hkuto/record.jsp?B19588999.

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卞勁松 and Jin-song Bian. "The role of protein kinase C upon K-opioid receptor stimulation in theheart." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31239900.

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Klipp, Robert Carl. "Catecholamine Interactions with the Cardiac Ryanodine Receptor." PDXScholar, 2013. https://pdxscholar.library.pdx.edu/open_access_etds/1439.

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The cardiac ryanodine receptor (RyR2) is a Ca2+ ion channel found in the sarcoplasmic reticulum (SR), an intracellular membranous Ca2+ storage system. It is well known that a destabilization of RyR2 can lead to a Ca2+ flux out of the SR, which results in an overload of intracellular Ca2+; this can also lead to arrhythmias and heart failure. The catecholamines play a large role in the regulation of RyR2; stimulation of the Beta-adrenergic receptor on the cell membrane can lead to a hyperphosphorylation of RyR2, making it more leaky to Ca2+. We have previously shown that strong electron donors will inhibit RyR2. It is hypothesized that the catecholamines, sharing a similar structure with other proven inhibitors of RyR2, will also inhibit RyR2. Here we confirm this hypothesis and show for the first time that the catecholamines, isoproterenol and epinephrine, act as strong electron donors and inhibit RyR2 activity at the single channel level. This data suggests that the catecholamines can influence RyR2 activity at two levels. This offers promising insight into the potential development of a new class of drugs to treat heart failure and arrhythmia; ones that can both prevent the hyperphosphorylation of RyR2 by blocking the Beta;-adrenergic receptor, but can also directly inhibit the release of Ca2+ from RyR2.

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NAGATA, KOHZO, TOYOAKI MUROHARA, XIAN WU CHENG, SHOGO WATANABE, MASAAKI MIYACHI, MAYUKO OHTAKE, MIWA TAKATSU, et al. "Glucocorticoids Activate Cardiac Mineralocorticoid Receptors in Adrenalectomized Dahl Salt- Sensitive Rats." Nagoya University School of Medicine, 2014. http://hdl.handle.net/2237/19484.

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Books on the topic "Cardiac receptors"

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Gesellschaft für Fortschritte auf dem Gebiet der Inneren Medizin. Symposium. Cardiovascular receptors: New pharmacological and clinical aspects : 18th Symposium of the Gesellschaft für Fortschritte auf dem Gebiet der Inneren Medizin, Düsseldorf, December 1984 (chairman: Paul Schölmerich with collaboration of Erland Erdmann and Hasso Scholz). Stuttgart: G. Thieme, 1986.

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van, Zwieten P. A., and Schönbaum E, eds. Receptors in the cardiovascular system: Proceedings of a symposium, organized by the Dutch Pharmacological Society in OSS, the Netherlands, May 31, 1985. New York: G. Fischer Varlag, 1986.

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Cardiac Glycoside Receptors and Positive Inotropy: Evidence for More Than One Receptor? Springer, 1986.

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Rosenbaum, Larry C. Structural characterization of the cardiac muscarinic acetylcholine receptor. 1987.

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Ernst E. van der Wall, P. K. Blanksma, and M. G. Niemeyer. Cardiac Positron Emission Tomography: Viability, Perfusion, Receptors and Cardiomyopathy. Springer, 2012.

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Chidiac, Peter. Cardiac muscarinic receptors and G proteins: mechanism of interaction. 1992.

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Wall, Ernst E. van der, P. K. Blanksma, M. G. Niemeyer, and A. M. Paans. Cardiac Positron Emission Tomography: Viability, Perfusion, Receptors and Cardiomyopathy. Springer, 2012.

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8

Cardiac positron emission tomography: Viability, perfusion, receptors, and cardiomyopathy. Dordrecht: Kluwer Academic Publishers, 1995.

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Blanksma, P. K., A. M. Paans, Ernst E. van der Wall, and M. G. Niemeyer. Cardiac Positron Emission Tomography: Viability, Perfusion, Receptors and Cardiomyopathy. Springer London, Limited, 2012.

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Green, Marty Anne *. The binding properties of muscarinic receptors in washed cardiac membranes. 1988.

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Book chapters on the topic "Cardiac receptors"

1

Nguyen, Geneviève, Céline Burckle, and Benjamin Tremey. "The Cardiac Renin Receptors." In Renin Angiotensin System and the Heart, 75–83. Chichester, UK: John Wiley & Sons, Ltd, 2006. http://dx.doi.org/10.1002/0470032103.ch6.

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Guyonnet, Jérôme. "Serotonin and Cardiac Valves Degeneration in Dog." In 5-HT2B Receptors, 189–211. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-55920-5_11.

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Saraste, Antti, Hossam Sherif, and Markus Schwaiger. "PET Innervation and Receptors." In Cardiac CT, PET and MR, 140–53. Oxford, UK: Wiley-Blackwell, 2010. http://dx.doi.org/10.1002/9781444323894.ch6.

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Miyamoto, Shigeki, Sunny Yang Xiang, Nicole H. Purcell, and Joan Heller Brown. "Mechanisms and Models for Elucidating the Cardiac Effects of Sphingosine 1-Phosphate (S1P)." In Lysophospholipid Receptors, 373–97. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2013. http://dx.doi.org/10.1002/9781118531426.ch17.

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Perrino, Cinzia, and Howard A. Rockman. "Modulating G Protein-Coupled Receptors to Effect Reverse Cardiac Remodeling." In Cardiac Remodeling, 159–77. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-5930-9_10.

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Frantz, Stefan, Ralph A. Kelly, and Todd Bourcier. "Toll-like receptors and the cardiovascular system." In Inflammation and Cardiac Diseases, 129–41. Basel: Birkhäuser Basel, 2003. http://dx.doi.org/10.1007/978-3-0348-8047-3_8.

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Justus, David E., Adam Hoffman, Ekaterina Mironova, Alexander Hartman, Jack G. Goldsmith, Jay D. Potts, and Edie C. Goldsmith. "Discoidin Domain Receptors in Cardiac Development." In Discoidin Domain Receptors in Health and Disease, 331–47. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6383-6_18.

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Lohse, M. J., and S. Engelhardt. "Cardiac overexpression of β-adrenergic receptors." In Molecular Approaches to Heart Failure Therapy, 26–38. Heidelberg: Steinkopff, 2000. http://dx.doi.org/10.1007/978-3-642-57710-9_3.

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Schmidt, Thomas A., and Keld Kjeldsen. "Regulation of Digitalis Glycoside Receptors in Digoxin Treatment." In Cardiac Remodeling and Failure, 501–10. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4419-9262-8_34.

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Valette, Heric, Andre Syrota, and Pascal Merlet. "Use of PET Radiopharmaceuticals to Probe Cardiac Receptors." In Cardiac Positron Emission Tomography, 331–51. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-1233-8_18.

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Conference papers on the topic "Cardiac receptors"

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Vallmitjana, A., C. Nolla, A. Herraiz-Martinez, L. Hove-Madsen, and R. Benitez. "Spatial localization of ryanodine receptors in human cardiac cells." In 2015 37th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2015. http://dx.doi.org/10.1109/embc.2015.7319832.

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Knuefermann, P., R. Lohner, O. Boehm, M. Schwederski, R. Meyer, and G. Baumgarten. "Cardiac Inflammation and Function during Polymicrobial Sepsis: Differential Role of Toll-Like Receptors." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a1146.

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Mylvaganam, R., L. Colangelo, R. Ramasubramanian, B. Thyagarajan, D. Jacobs, M. Gross, R. Kalhan, S. Khan, and M. J. Cuttica. "Cardiac Mechanics and Gene Expression of Pathogen Recognition Pathway Receptors: The Coronary Artery Risk Development in Young Adults (CARDIA) Study." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a5163.

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Lee, S., JH Boyd, Y. Wang, and KR Walley. "Hsp70 Mediates Inflammatory Cardiac Dysfunction Via Toll-Like Receptors: Link between Innate Immune Modulators and Cardiomyocyte Contractility." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5741.

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Gallagher, L., M. McCusker, M. Chemaly, A. Peace, M. Gibson, AJ Bjourson, C. Kelly, and VE McGilligan. "54 The nlrp3 inflammasome and other related receptors as potential biomarkers in coronary artery disease (cad) and major adverse cardiac events (mace)." In Irish Cardiac Society Annual Scientific Meeting & AGM, Thursday October 5th – Saturday October 7th 2017, Millennium Forum, Derry∼Londonderry, Northern Ireland. BMJ Publishing Group Ltd and British Cardiovascular Society, 2017. http://dx.doi.org/10.1136/heartjnl-2017-ics17.54.

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Shabaldin, A. V., L. N. Igisheva, and A. A. Rumyanceva. "CONTRIBUTION OF GENETIC PREDICTORS TO FORMATION OF HEALTH DEFICIENCY IN THE SEPARATE PERIOD AFTER CARDIAC SURGERY TREATMENT OF CONGENITAL HEART DEFECTS." In I International Congress “The Latest Achievements of Medicine, Healthcare, and Health-Saving Technologies”. Kemerovo State University, 2023. http://dx.doi.org/10.21603/-i-ic-151.

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Objective: To study the contribution of xenobiotic biotransformation enzyme genes, transcription factors, inflammatory and immune response receptors in determining health deficiency in the separated period after cardiac surgery for congenital heart disease. Materials and methods. 116 children who underwent radical correction of CHD were examined. An assessment of the catamnesis of these children and genetic typing of genes encoding enzymes for the biotransformation of xeno- and endobiotics (GSTP, CYP1A2, CYP1A1), involved in the determination of cardiogenesis and processes in cardiomyocytes (CRELD-1, GATA-6, NOTCH-1), innate ( TREM-1) and adaptive (HLA-DR) immunity. The search for predictors of functioning deficit by physical, psycho-emotional, social, mental types was carried out using multiple logistic regression. Results. The level of functioning of various components of health one year after surgical treatment was associated with the same factors. These factors negatively affecting the health of children one year after heart surgery were: unfavorable living conditions, as well as genetic predictor markers HLA-DRB1*07 and Creld1 T/C (rs9878047)*T.

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TEIXEIRA, GUILHERME PEGAS, and ROBSON XAVIER FARIA. "INIBIÇÃO DO RECEPTOR PURINÉRGICO P2X7 COMO UMA NOVA ESTRATÉGIA CONTRA DIABETES TIPO 2." In I Congresso Brasileiro de Doenças Crônicas On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/cronics/7456.

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Introdução: A sinalização purinérgica é um sistema de receptores de membrana ativados por purinas, envolvidos em diversos processos fisiológicos e patológicos do organismo. O receptor purinérgico P2X7 é o mais marcante neste sistema. Trata-se de um receptor ionotrópico ativado por adenosina trifosfato (ATP) extracelular com ampla participação na resposta imunológica e na liberação das citocinas pró-inflamatórias IL-1 e IL-18. A superprodução destes mediadores induz resistência à insulina no tecido adiposo e muscular esquelético através da diminuição do transportador de glicose dependente de insulina GLUT 4, fator este que pode levar ao surgimento da diabetes tipo 2. Objetivo: Apresentar a influência do receptor P2X7 como nova estratégia farmacológica na diabetes tipo 2. Metodologia: Foram selecionados seis trabalhos publicados na literatura dos últimos dez anos. As palavras-chave: receptor P2X7, inflamação, resistência à insulina e diabetes tipo 2 foram usadas em diferentes combinações para a seleção dos artigos. Resultados: Durante a diabetes tipo 2, ácidos graxos livres (AGLs) em excesso levam a complicações no metabolismo da glicose. Os AGLs induzem a transcrição das formas imaturas de IL-1 e IL-18 por meio da sinalização via receptor Toll Like 4. Com o aumento de ATP extracelular, o P2X7 é ativado, promovendo o processo inflamatório através da maturação e liberação das citocinas IL-1 e IL-18 pela sinalização Nod Like Receptor protein 3. Estes mediadores desregulam a fosforilação do substrato do receptor de insulina IRS, diminuindo a translocação de GLUT 4 a membrana plasmática, desta forma aumentando a glicemia sanguínea. Estudos em camundongos C57BL/6 mostraalterações nos parâmetros cardíacos induzidos pela alta concentração de glicose, levando a processos de remodelação cardíaca e estresse oxidativo. Interessantemente, estes quadros foram melhorados com a inibição farmacológica do receptor P2X7. Neste contexto, antagonistas do receptor P2X7 foram utilizados em ensaios clínicos, como as moléculas AZD9056 e CE-224,535 para doenças inflamatórias, mostrando boa tolerabilidade. Desta forma, estes são exemplos de antagonistas que podem ser utilizados em estudos de desordens metabólicas. Conclusão: O receptor P2X7 induz o processo inflamatório na diabetes levando a desregulação da sinalização da insulina. Estratégias utilizando antagonistas deste receptor podem ser promissoras no tratamento da diabetes tipo 2.

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Schenkl, C., A. Schrepper, D. Gonzalez-Lopez, D. Wanjek, M. Schwarzer, and T. Doenst. "IGF-1 Receptor Inhibition Causes Reversible Cardiac Atrophy and Contractile Dysfunction." In 48th Annual Meeting German Society for Thoracic, Cardiac, and Vascular Surgery. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1678820.

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Gollmann-Tepeköylü, C., M. Graber, L. Pölzl, J. Hirsch, F. Nägele, D. Lobenwein, V. Sladky, et al. "Thoracic Radiation Induces Toll-Like Receptor–Mediated Calcific Aortic Valve Disease." In 48th Annual Meeting German Society for Thoracic, Cardiac, and Vascular Surgery. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1678990.

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Mauer, J., A. Kuckhahn, J. Distler, B. Spriewald, M. Ramsperger-Gleixner, S. Ensminger, M. Weyand, and C. Heim. "Receptor Tyrosine Kinase Inhibitor Nintedanib as Treatment Option in Bronchiolitis Obliterans after Lung Transplantation." In 48th Annual Meeting German Society for Thoracic, Cardiac, and Vascular Surgery. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1678898.

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Reports on the topic "Cardiac receptors"

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Klipp, Robert. Catecholamine Interactions with the Cardiac Ryanodine Receptor. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.1438.

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2

Fukuta, Hidekatsu, Hiromi Hagiwara, and Takeshi Kamiya. Effects of angiotensin-receptor neprilysin inhibitor on exercise capacity, quality of life, and cardiac function in heart failure with preserved ejection fraction: a protocol for meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2021. http://dx.doi.org/10.37766/inplasy2021.7.0076.

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