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Relevant bibliographies by topics / Endothelium and hyperpolarizing factors

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Academic literature on the topic 'Endothelium and hyperpolarizing factors'

Author: Grafiati

Published: 7 June 2025

Last updated: 26 June 2025

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Journal articles on the topic "Endothelium and hyperpolarizing factors"

1

Sandow, Shaun L. "Factors, fiction and endothelium-derived hyperpolarizing factor." Clinical and Experimental Pharmacology and Physiology 31, no. 9 (2004): 563–70. http://dx.doi.org/10.1111/j.1440-1681.2004.04048.x.

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Janssen, Luke J. "Are endothelium-derived hyperpolarizing and contracting factors isoprostanes?" Trends in Pharmacological Sciences 23, no. 2 (2002): 59–62. http://dx.doi.org/10.1016/s0165-6147(02)01890-4.

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Campbell, William B., and John R. Falck. "Arachidonic Acid Metabolites as Endothelium-Derived Hyperpolarizing Factors." Hypertension 49, no. 3 (2007): 590–96. http://dx.doi.org/10.1161/01.hyp.0000255173.50317.fc.

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Campbell, William B., and Kathryn M. Gauthier. "What is new in endothelium-derived hyperpolarizing factors?" Current Opinion in Nephrology and Hypertension 11, no. 2 (2002): 177–83. http://dx.doi.org/10.1097/00041552-200203000-00008.

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FARACI, FRANK M., and DONALD D. HEISTAD. "Regulation of the Cerebral Circulation: Role of Endothelium and Potassium Channels." Physiological Reviews 78, no. 1 (1998): 53–97. http://dx.doi.org/10.1152/physrev.1998.78.1.53.

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Faraci, Frank M., and Donald D. Heistad. Regulation of the Cerebral Circulation: Role of Endothelium and Potassium Channels. Physiol. Rev. 78: 53–97, 1998. — Several new concepts have emerged in relation to mechanisms that contribute to regulation of the cerebral circulation. This review focuses on some physiological mechanisms of cerebral vasodilatation and alteration of these mechanisms by disease states. One mechanism involves release of vasoactive factors by the endothelium that affect underlying vascular muscle. These factors include endothelium-derived relaxing factor (nitric oxide), prostacyclin, and endothelium-derived hyperpolarizing factor(s). The normal vasodilator influence of endothelium is impaired by some disease states. Under pathophysiological conditions, endothelium may produce potent contracting factors such as endothelin. Another major mechanism of regulation of cerebral vascular tone relates to potassium channels. Activation of potassium channels appears to mediate relaxation of cerebral vessels to diverse stimuli including receptor-mediated agonists, intracellular second messengers, and hypoxia. Endothelial- and potassium channel-based mechanisms are related because several endothelium-derived factors produce relaxation by activation of potassium channels. The influence of potassium channels may be altered by disease states including chronic hypertension, subarachnoid hemorrhage, and diabetes.

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Baskakov, M. B., and M. S. Yusubov. "Gas attack or gently, the gases!" Bulletin of Siberian Medicine 9, no. 6 (2010): 160–64. http://dx.doi.org/10.20538/1682-0363-2010-6-160-164.

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The article contains the current understanding of gas communication in smooth muscle cells, the basic mechanisms of action of gaseous transmitters, analyzes the different views on the nature of the endothelial relaxing and endothelial hyperpolarizing factors. We discuss the controversial issues of the mechanisms of endothelium-dependent relaxation of vascular smooth muscle.

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McGuire, John J., Hong Ding, and Chris R. Triggle. "Endothelium-derived relaxing factors: A focus on endothelium-derived hyperpolarizing factor(s)." Canadian Journal of Physiology and Pharmacology 79, no. 6 (2001): 443–70. http://dx.doi.org/10.1139/y01-025.

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Endothelium-derived hyperpolarizing factor (EDHF) is defined as the non-nitric oxide (NO) and non-prostacyclin (PGI2) substance that mediates endothelium-dependent hyperpolarization (EDH) of vascular smooth muscle cells (VSMC). Although both NO and PGI2 have been demonstrated to hyperpolarize VSMC by cGMP- and cAMP-dependent mechanisms, respectively, and in the case of NO by cGMP-independent mechanisms, a considerable body of evidence suggests that an additional cellular mechanism must exist that mediates EDH. Despite intensive investigation, there is no agreement as to the nature of the cellular processes that mediates the non-NO/PGI2 mediated hyperpolarization. Epoxyeicosatrienoic acids (EET), an endogenous anandamide, a small increase in the extracellular concentration of K+, and electronic coupling via myoendothelial cell gap junctions have all been hypothesized as contributors to EDH. An attractive hypothesis is that EDH is mediated via both chemical and electrical transmissions, however, the contribution from chemical mediators versus electrical transmission varies in a tissue- and species-dependent manner, suggesting vessel-specific specialization. If this hypothesis proves to be correct then the potential exists for the development of vessel and organ-selective vasodilators. Because endothelium-dependent vasodilatation is dysfunctional in disease states (i.e., atherosclerosis), selective vasodilators may prove to be important therapeutic agents.Key words: endothelium, nitric oxide, potassium channels, hyperpolarization, gap junctions.

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Campbell, William B., Debebe Gebremedhin, Phillip F. Pratt, and David R. Harder. "Identification of Epoxyeicosatrienoic Acids as Endothelium-Derived Hyperpolarizing Factors." Circulation Research 78, no. 3 (1996): 415–23. http://dx.doi.org/10.1161/01.res.78.3.415.

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Khalil, Raouf A., and Joey P. Granger. "Vascular mechanisms of increased arterial pressure in preeclampsia: lessons from animal models." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 283, no. 1 (2002): R29—R45. http://dx.doi.org/10.1152/ajpregu.00762.2001.

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Normal pregnancy is associated with reductions in total vascular resistance and arterial pressure possibly due to enhanced endothelium-dependent vascular relaxation and decreased vascular reactivity to vasoconstrictor agonists. These beneficial hemodynamic and vascular changes do not occur in women who develop preeclampsia; instead, severe increases in vascular resistance and arterial pressure are observed. Although preeclampsia represents a major cause of maternal and fetal morbidity and mortality, the vascular and cellular mechanisms underlying this disorder have not been clearly identified. Studies in hypertensive pregnant women and experimental animal models suggested that reduction in uteroplacental perfusion pressure and the ensuing placental ischemia/hypoxia during late pregnancy may trigger the release of placental factors that initiate a cascade of cellular and molecular events leading to endothelial and vascular smooth muscle cell dysfunction and thereby increased vascular resistance and arterial pressure. The reduction in uterine perfusion pressure and the ensuing placental ischemia are possibly caused by inadequate cytotrophoblast invasion of the uterine spiral arteries. Placental ischemia may promote the release of a variety of biologically active factors, including cytokines such as tumor necrosis factor-α and reactive oxygen species. Threshold increases in the plasma levels of placental factors may lead to endothelial cell dysfunction, alterations in the release of vasodilator substances such as nitric oxide (NO), prostacyclin (PGI2), and endothelium-derived hyperpolarizing factor, and thereby reductions of the NO-cGMP, PGI2-cAMP, and hyperpolarizing factor vascular relaxation pathways. The placental factors may also increase the release of or the vascular reactivity to endothelium-derived contracting factors such as endothelin, thromboxane, and ANG II. These contracting factors could increase intracellular Ca2+concentrations ([Ca2+]i) and stimulate Ca2+-dependent contraction pathways in vascular smooth muscle. The contracting factors could also increase the activity of vascular protein kinases such as protein kinase C, leading to increased myofilament force sensitivity to [Ca2+]i and enhancement of smooth muscle contraction. The decreased endothelium-dependent mechanisms of vascular relaxation and the enhanced mechanisms of vascular smooth muscle contraction represent plausible causes of the increased vascular resistance and arterial pressure associated with preeclampsia.

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Villar, Inmaculada C., Adrian J. Hobbs, and Amrita Ahluwalia. "Sex differences in vascular function: implication of endothelium-derived hyperpolarizing factor." Journal of Endocrinology 197, no. 3 (2008): 447–62. http://dx.doi.org/10.1677/joe-08-0070.

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The vascular endothelium plays a crucial role in the regulation of vascular homeostasis by controlling vascular tone, coagulation, and inflammatory responses. These actions are exerted by endothelial factors including nitric oxide, prostacyclin, and endothelium-derived hyperpolarizing factor (EDHF). The greater incidence of cardiovascular disease (CVD) in men and postmenopausal women compared with premenopausal women implies a vasoprotective phenotype of females, which may be influenced by sex hormones. These hormones, particularly estrogen, have modulatory effects on the endothelium and circulating cells that have been implicated in vascular inflammation and in the development of CVD. EDHF seems to be the predominant endothelial factor in the resistance vasculature of females and this mediator could afford the beneficial cardiovascular risk profile observed in premenopausal woman. In this review, we discuss sex differences in EDHF biology and how sex hormones can modulate EDHF responses. We also review the implication of sex hormone-dependent regulation of EDHF in inflammatory processes, platelet function, and repair after vascular damage, each of which have a critical role in several aspects of the pathogenesis of CVD.

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Dissertations / Theses on the topic "Endothelium and hyperpolarizing factors"

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Burnette, Ethan Williams. "Endothelium-derived hyperpolarizing factor (EDHF) in rat mesenteric artery." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/NQ66130.pdf.

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Kenny, Louise Clare. "The role of endothelium-derived hyperpolarizing factor in normal and compromised pregnancies." Thesis, University of Nottingham, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.289067.

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McNeish, Alister J. "Inhibition of endothelium-derived hyperpolarizing factor by ascorbate in the bovine eye." Thesis, University of Glasgow, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.252519.

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Nagaraja, Sridevi. "Theoretical Investigations of Communication in the Microcirculation: Conducted Responses, Myoendothelial Projections and Endothelium Derived Hyperpolarizing Factor." FIU Digital Commons, 2011. http://digitalcommons.fiu.edu/etd/520.

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The contractile state of microcirculatory vessels is a major determinant of the blood pressure of the whole systemic circulation. Continuous bi-directional communication exists between the endothelial cells (ECs) and smooth muscle cells (SMCs) that regulates calcium (Ca2+) dynamics in these cells. This study presents theoretical approaches to understand some of the important and currently unresolved microcirculatory phenomena. Agonist induced events at local sites have been shown to spread long distances in the microcirculation. We have developed a multicellular computational model by integrating detailed single EC and SMC models with gap junction and nitric oxide (NO) coupling to understand the mechanisms behind this effect. Simulations suggest that spreading vasodilation mainly occurs through Ca2+ independent passive conduction of hyperpolarization in RMAs. Model predicts a superior role for intercellular diffusion of inositol (1,4,5)-trisphosphate (IP3) than Ca2+ in modulating the spreading response. Endothelial derived signals are initiated even during vasoconstriction of stimulated SMCs by the movement of Ca2+ and/or IP3 into the EC which provide hyperpolarizing feedback to SMCs to counter the ongoing constriction. Myoendothelial projections (MPs) present in the ECs have been recently proposed to play a role in myoendothelial feedback. We have developed two models using compartmental and 2D finite element methods to examine the role of these MPs by adding a sub compartment in the EC to simulate MP with localization of intermediate conductance calcium activated potassium channels (IKCa) and IP3 receptors (IP3R). Both models predicted IP3 mediated high Ca2+ gradients in the MP after SMC stimulation with limited global spread. This Ca2+ transient generated a hyperpolarizing feedback of ~ 2-3mV. Endothelium derived hyperpolarizing factor (EDHF) is the dominant form of endothelial control of SMC constriction in the microcirculation. A number of factors have been proposed for the role of EDHF but no single pathway is agreed upon. We have examined the potential of myoendothelial gap junctions (MEGJs) and potassium (K+) accumulation as EDHF using two models (compartmental and 2D finite element). An extra compartment is added in SMC to simulate micro domains (MD) which have NaKα2 isoform sodium potassium pumps. Simulations predict that MEGJ coupling is much stronger in producing EDHF than alone K+ accumulation. On the contrary, K+ accumulation can alter other important parameters (EC Vm, IKCa current) and inhibit its own release as well as EDHF conduction via MEGJs. The models developed in this study are essential building blocks for future models and provide important insights to the current understanding of myoendothelial feedback and EDHF.

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Chow, Kin-hong, and 周健航. "Role of nitric oxide in the regulation of vascular responses mediated by prostaglandin and endothelium-derived hyperpolarizing factor in theporcine coronary artery." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B46699429.

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Sheng, Huan. "Factors affecting corneal endothelial morphology." Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1141395542.

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Yong, Kwee Lan. "The effects of myeloid growth factors on phagocyte-endothelium interactions." Thesis, University College London (University of London), 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.388120.

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Randall, Michael David. "Activities of endothelium-derived vasoactive factors in resistance beds of the rat." Thesis, University of Cambridge, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.315052.

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Cuhlmann, Simon. "Effects of shear stress on NF-κB transcription factors in vascular endothelium". Thesis, Imperial College London, 2011. http://hdl.handle.net/10044/1/6440.

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Atherosclerosis, a chronic inflammatory disease of arteries, occurs predominantly at regions of the arterial system that are exposed to disturbed patterns of blood flow. Blood flow influences the atherosclerosis by exerting shear stress on endothelial cells (ECs). Although the signalling pathways that activate pro-inflammatory NF-κB transcription factors are well defined, the regulation and physiological significance of differential NF-κB subunit expression is poorly understood. In this thesis, we demonstrate that RelA NF-κB sub-unit expression is positively regulated in ECs via c-Jun N-terminal kinase (JNK) and the transcription factor ATF2. This pathway promoted focal arterial inflammation as genetic deletion of JNK1 reduced RelA expression and macrophage accumulation at an athero-susceptible site. Furthermore, JNK signalling to RelA is controlled by mechanical forces as en face immunostaining revealed that disturbed flow patterns (generated by a constrictive cuff) elevated RelA expression in murine carotid arteries via JNK1. Positron emission tomography and en face staining revealed that disturbed flow enhanced 18F-fluorodeoxyglucose uptake (a marker of inflammation) and accumulation of CD68-positive inflammatory cells in arteries via JNK1. We conclude that disturbed flow promotes arterial inflammation via a novel JNK-NF-κB cross-talk. The duration of RelA nuclear localisation is an important determinant of the magnitude and specificity of target gene expression. En face staining revealed that RelA rapidly accumulated in the nucleus upon LPS stimulation in ECs at both athero-protected and athero-susceptible sites. RelA was exported from the nucleus to the cytoplasm in response to prolonged stimulation in the athero-protected region but not in the athero-susceptible region. The duration of RelA nuclear localisation was suppressed by histone deacetylases which displayed higher activity at the protected site compared to the susceptible site. Overall, our findings reveal that ECs at athero-susceptible sites are primed for inflammatory activation via complementary mechanisms that enhance both the expression and the activity of NF-κB transcription factors.

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Ku, Chun-Ying. "Colony-Stimulating Factor from Umbilical Cord Endothelial Cells." Thesis, North Texas State University, 1987. https://digital.library.unt.edu/ark:/67531/metadc935638/.

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Conditioned media prepared from umbilical cord (UC) segments or endothelial cells (EC) contain colony stimulating activity, Both UCCM and ECCM were partially purified by DEAE-Sepharose and ACA44 gel filtration chromatography. The molecular weights were estimated as 25,000 and 31,000 for UC-CSF and EC-CSF, respectively. UC-CSF was further fractionated by Con A Sepharose, IEF and HPLC on a hydrophobic phenyl column. The highly purified CSF stimulates human macrophage and granulocyte colony formation, indicating it is GM-CSF in nature. Characterization studies have revealed that both CSFs are heat stable at 60°C for 30 min. They are sensitive to digestion by protease and to periodate oxidation but are stable to treatment with sulfhydryl reagents. The synthesis of CSF in endothelial cells is inhibited by actinomycin D, cycloheximide and puromycin, indicating that protein and RNA synthesis are required for CSF production. Among the mitogens tested, only LPS exhibited stimulatory activity on the production of CSF. Metabolic modulators such as dibutyryl cAMP, isobutylmethylxanthine, PGE2 and lactoferrin inhibit CSF production, while PGF2 enhances CSF production.

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Books on the topic "Endothelium and hyperpolarizing factors"

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M, Vanhoutte Paul, ed. Endothelium-derived hyperpolarizing factor. Harwood Academic Publishers, 1996.

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International Symposium on Endothelium-Derived Vasoactive Factors (1st 1989 Philadelphia, Pa.). Endothelium-derived contracting factors. Edited by Rubanyi Gabor M. 1947-, Vanhoutte Paul M, and International Symposium on Endothelium-Derived Vasoactive Factors (1st : 1989 : Philadelphia, Pa.). Karger, 1990.

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International Symposium on Endothelium-Derived Vasoactive Factors (1st 1989 Philadelphia, Pa.). Endothelium-derived relaxing factors. Edited by Rubanyi Gabor M. 1947-, Vanhoutte Paul M, and International Symposium on Endothelium-Derived Vasoactive Factors (1st : 1989 : Philadelphia, Pa.). Karger, 1990.

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Tousoulis, Dimitris. Risk factors and vascular endothelium. Nova Science Publishers, 2011.

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1947-, Rubanyi Gabor M., ed. Cardiovascular significance of endothelium-derived vasoactive factors. Futura Pub. Co., 1991.

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Tomoh, Masaki, ed. Endothelium-derived factors and vascular functions: Proceedings of the Fourth International Symposium on Endothelium-Derived Factors, Tokyo, 7-9 December, 1993. Excerpta Medica, 1994.

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Job, Harenberg, and Heidelberger Akademie der Wissenschaften, eds. New trends in haemostasis: Coagulation proteins, endothelium, and tissue factors. Springer-Verlag, 1990.

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V, Schaff Hartzell, ed. Vasoactive factors produced by the endothelium: Physiology and surgical implications. R.G. Landes, 1994.

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1941-, Ryan Una S., and Rubanyi Gabor M. 1947-, eds. Endothelial regulation of vascular tone. M. Dekker, 1992.

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C, Weber Peter, and Leaf Alexander 1920-, eds. Atherosclerosis: Cellular interactions, growth factors, and lipids. Raven Press, 1993.

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Book chapters on the topic "Endothelium and hyperpolarizing factors"

1

Edwards, Gillian, and Arthur H. Weston. "Endothelium-derived hyperpolarizing factor — a critical appraisal." In Progress in Drug Research. Birkhäuser Basel, 1998. http://dx.doi.org/10.1007/978-3-0348-8833-2_2.

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Triggle, Chris R., Malarvannan Pannirselvam, Todd J. Anderson, and Hong Ding. "Endothelium-Derived Hyperpolarizing Factor(s). Does it Exist and What Role Does it Play in the Regulation of Blood Flow?" In Pathophysiology of Cardiovascular Disease. Springer US, 2004. http://dx.doi.org/10.1007/978-1-4615-0453-5_25.

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Allayee, Hooman, Brad Aouizerat, Richard Davis, et al. "Genetic Factors in Atherosclerosis." In Vascular Endothelium. Springer US, 1998. http://dx.doi.org/10.1007/978-1-4899-0133-0_12.

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Gao, Yuansheng. "Endothelium-Derived Factors." In Biology of Vascular Smooth Muscle: Vasoconstriction and Dilatation. Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-4810-4_8.

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Gao, Yuansheng. "Endothelium-Derived Factors." In Biology of Vascular Smooth Muscle. Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-7122-8_8.

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Vanhoutte, Paul M., Thomas Gräser, and Thomas F. Lüscher. "Endothelium-Derived Contracting Factors." In Endothelin. Springer New York, 1992. http://dx.doi.org/10.1007/978-1-4614-7514-9_1.

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Block, Edward R. "Factors Affecting the Fluidity of the Endothelial Cell Plasma Membrane." In Vascular Endothelium. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-8532-5_3.

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Houston, Donald S., and Paul M. Vanhoutte. "Platelets and Endothelium-Dependent Responses." In Relaxing and Contracting Factors. Humana Press, 1988. http://dx.doi.org/10.1007/978-1-4612-4588-9_21.

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Nagy, Z., K. Kolev, M. Pék, É. Csorkia, M. Vastag, and R. Machovich. "Human Brain Endothelial Cell-Contraction Induced by Hemostasis and Fibrinolysis Factors, In Vitro Cell Culture Study." In Vascular Endothelium. Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-0355-8_64.

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Furchgott, Robert F. "Endothelium-Dependent Relaxation in Systemic Arteries." In Relaxing and Contracting Factors. Humana Press, 1988. http://dx.doi.org/10.1007/978-1-4612-4588-9_1.

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Conference papers on the topic "Endothelium and hyperpolarizing factors"

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Chamone, D. A. F., A. Y. Hoshikawa-Fujimura, C. Massumoto, G. Bellotti, F. Arashiro, and M. Jamra. "ABNORMALITIES OF PLATELET AGGREGATION AND ENHANCED FACTOR X ACTIVATOR ACTIVITY OF WASHED PLATELETS IN SICKLE CELL DISEASE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644544.

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The occurence of microvascular occlusion is one of the most prominent pathologic features of sickle cell anemia. The mechanism of vaso occlusion has generally been attributed to the abnormal shape and reduced deformability of the sickled erithrocy tes. However, the involvement of vascular endothelium, platelets and their interactions with coagulation factors may also be of pathogenic significance in microvascular occlusive crises.We investigated the interaction between vascular endothelium, platelets and blood coagulation factors in 23 patients with Sickle Cell Disease (SCD) and in normal volunteers.Factor X activator activity in washed platelets was performed according to Semeraro and Vermylen (1977), thromboxane B2 (TXB2) and 6-keto-PGF1β were determined using specific radioimmunoassays.. PAF-acether from platelets was determined according to Chignard et al (Nature, 1979, 279:799). Platelet aggregation was performed with a Chrono-Log Aggregometer (Model 440) on platelet rich plasma (PRP) using the Born method. Prostacyclin release from endothelium was performed according to Mon-cada et al (Lancet i:18, 1977).Our results showed that platelets from patients with SCD ha ve enhanced factor X activator activity (p < 0.0001), produce mo re PAF-acether than controls (p < 0.02) and showed hyperaggregability in these patients as compared to normal volunteers (p < 0.00001).We concluded that platelets from homozygous sicklers have enhanced factor X activator activity as well as increased capacity for PAF-acether production. These abnormalities may contribute to the incidence of vaso occlusive crises in these patients.

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Stern, David M., Sara Rimon, Todd Scott, and Peter P. Nawroth. "MODULATION OF ENDOTHELIAL CELL COAGULANT PROPERTIES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642946.

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As the cells forming the luminal vascular surface, endothelium is strategically located to play a role in the regulation of coagulation. Participation of endothelium in coagulation involves specific receptors on the cell surface functioning at the level of initiation and propagation of hemostatic reactions. In the anticoagulant protein C pathway, for example, the receptor thrombomodulin initiates thrombin-mediated activation of protein C and a binding site for protein S on bovine endothelium promotes assembly of the functional activated protein C/protein S complex. Endothelium also synthesizes, stores and releases functional protein S constitutively and in response to specific stimuli such as norepinephrine.Since activation of protein C requires thrombin formation in proximity to the vessel wall, we have examined procoagulant reactions on the endothelial cell surface. Endothelium provides a receptor for Factor IX/IXa which is relatively selective for the enzyme form and facilitates Factor IXa-VIII-mediated activation of Factor X. Half-maximal Factor Xa formation occurs at a Factor IXa concentration of 0.4nM on endothelium, whereas lOnM is required on liposomes. This concentration of Factor IXa corresponds to that which results in half-maximal occupancy of endothelial cell Factor IXa binding sites in the presence of Factors VIII and X, thus correlating kinetics and binding measurements. Crosslinking and ligand blotting studies have shown that the receptor is a protein with a molecular weight of ∼160,000. The clinical significance of this receptor is suggested by the moderately severe bleeding disorder observed in a patient with hemophilia B due to an abnormal Factor IX molecule, Factor IXalabama (Factor IXala). Although the coagulant activity of Factor IXala is only mildly decreased on phospholipids, it is severely impaired on endothelium. The affinity of Factor IXala for the endothelial cell Factor X activation complex is decreased by 20-fold compared with the normal enzyme and the binding affinity is similarly decreased. Since the molecular defect in Factor IXala has been previously shown to consist of a single point mutation in the growth factor domain, this indicates a role for the growth factor domain in receptor, recognition.The picture of endothelial cell coagulant properties which emerges from these and other studies is one in which endothelium has either an anticoagulant or procoagulant potential, depending on modulation of receptor expression and release of secreted products. In the quiescent state, anticoagulant mechanisms predominate with only limited amounts of procoagulant activity: there is little tissue factor activity and only a basal level of receptors for Factor IX/lXa. Activation of endothelium by Tumor Necrosis Factor (TNF) or Interleukin 1 can shift this balance. Tissue factor synthesis and expression occurs in a dose-dependent manner, being half-maximal at a TNF concentration of about 150pM. TNF also increases the number of Factor IX/lXa binding sites. Concomitant with enhancement of endothelial cell procoagulant properties is a suppression of cell surface cofactor activity for the anticoagulant protein C pathway. Endothelial cell-dependent, thrombin-mediated activated protein C formation is decreased by 70-80% and activated protein C-protein S-mediated Factor Va inactivation decreases by over 90%. Following the in vivo infusion of Interleukin 1, similar changes in endothelial cell coagulant properties were observed on aortic segments with fibrin deposition occurring on the functionally altered, but morphologically intact endothelium. This modulation of endothelial cell coagulant properties could underlie the prothrombotic state associated with inflammatory disorders and could also explain the recently observed selective intravascular thrombosis of tumor vasculature seen in vivo in meth A sarcomas after administration of TNF.Thus, although endothelium was initially felt to be hemostatically inert, this apparent lack of activity actually masks a delicate balance of procoagulant and anticoagulant mechanisms. The balance can be effectively shifted by physiologic mediators, such as monokines, which alter receptor expression on the endothelial cell surface. Changes in endothelial cell hemostatic properties may be an early indicator of vessel wall disease and underlie the pathogenesis of localized thrombotic processes.

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Schen, Aaron, Baoguo Chen, and Lisa X. Xu. "Preliminary Study of Vascular Endothelial Ca2+ Response to Elevated Temperature." In ASME 2001 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2001. http://dx.doi.org/10.1115/imece2001/htd-24424.

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Abstract Local hyperthermia has been the subject of much research because of its great potential for therapeutic and clinic applications. It has been long recognized that a major factor, which affects tissue temperature elevation and heterogeneity during hyperthermia, is the augmentation of blood flow concomitant with the heating. The heat-induced change in local blood flow can be attributed to sympathetically mediated re-distribution of cardiac output and change in local flow resistance resulting from thermally stimulated regulation in diameters of arterioles. It has been found that the vascular endothelium significantly affects the dynamic response of the vessel diameter to thermal stimuli. Endothelial cells play key regulatory roles by producing several potent vasoactive agents and regulating coagulation states, i.e. endothelium derived relaxing factors (EDRFs). Most endothelial functions depend to various extents on changes in intracellular calcium concentration [Ca2+]i. A new approach to studying vascular thermo-regulation during hyperthermia has been developed in this research to quantitatively measure the dynamic response of vascular endothelial Ca2+ to temperature elevations using confocal fluorescence ratio imaging. The cell membrane permeable fluorescence dye Fura-2/AM esters were loaded into the vascular endothelial cells and ratio imaging of the fluorescent endothelial cell were taken under the excitation of 334 and 380nm wavelengths. The signal intensities were calibrated with the endothelial calcium ion concentration ([Ca2+]i) and temperatures ranged from 37°C to 44°C. This calibration will provide a means to quantitatively measure the vascular endothelial [Ca2+]i transients in in vivo tissue when subjected to temperature elevations from 38°C to 44°C, and thus to further understand the role of endothelium in thermally induced vascular regulation under hyperthermic conditions in the near future.

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Kim, Sungho, and Don P. Giddens. "Mass Transfer of LDL Based on Wall Shear Stress From FSI Simulation in Atherosclerotic Human Carotid Artery." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19661.

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Wall shear stress (WSS) distribution and low density lipoprotein (LDL) mass flux are simulated using a fluid-structure interaction (FSI) approach. T2 weighted black blood MRI images of a human left carotid artery are used for the arterial model construction, and the boundary conditions for FSI simulation are derived from phase contrast (PC) MR data. The endothelium is treated as a shear stress dependent, three pathways pore model for LDL particles. The computational results demonstrate that the region distal to an atherosclerotic plaque in the internal carotid artery experiences both low WSS and high mass and volume flux, which are hypothesized to be essential factors in progression of atherosclerosis.

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Drouet, L., G. Pignaud, L. Baladier, and C. Paris. "PLATELET INDUCED VASOSPASM." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644499.

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A new model of experimental thrombosis on 100 to 300 micron diameter rat mesenteric arteries has been designed.The focal specific deendothelialisation is induced by a tunable dye pulsed laser. All changes in the vascular lumen and of the vascular wall are observed under a stereozoom magnifier. This model allows in-time observation and quantification of induced phenomena after digitalisation and image processing of the video signal of the observation system. Besides thrombus formation and possibilities of its pharmacological manipulation, we focussed this study on the downstream vasospasm induced by platelet activation during thromboformation. The vasospasm is platelet dependent because it can be observed only when a platelet thrombus takes place . The vascular reaction is mediated through the endothelium, as the endothelium has been localy injured only on a 50 micron diameter spot at the place where the thrombus developpes and is intact at the level where the spasm is observed (more than 500 micro downstream). The role of platelet factors putatively involved in the vascular reaction has been evaluated by the use of specific inhibitors or antagonists (namely of ADP, serotonin, catecholamins, thromboxane A2 and PAF acether). Proofs are given that at least both platelet serotonin and thromboxane A2 are actively involved. These two intermediaries would sequentially participate : serotonin in the early phase and thromboxane A2 in the secondary phase. Vascular synthesis of prostacyclin does not seem to be a major intervenant in the regulation of the vascular tone.

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Weinbaum, Sheldon. "Mechano/Transduction, Cellular Communication and Fluid Flow in Tissue Engineering." In ASME 2000 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2000. http://dx.doi.org/10.1115/imece2000-2511.

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Abstract The growth of cellular constructs in tissue scaffolds depends on the delivery of nutrients and growth factors as well as the substrate on which they are grown. Micropatterning techniques have also made it possible to grow cells on a wide variety of substrates with greatly different topography which significantly alter cellular contact and communication. Fluid flow is critical not only in this delivery of nutrients and growth factors, but also in the interaction of the cell’s cytoskeleton with its attachment matrix. Similarly, fluid flow is known to play an important role in cell to cell communication via its regulatory effect on various gap junction proteins of the connexon family. The mechano/transduction and cell to cell signaling mechanisms will be examined for both cells with a smooth topography, such as vascular endothelium cells which are involved in angiogenesis and cells with cell processes and microvilli whose tethering attachments and protrusions interact with fluid flow in a different manner.

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Ye, Jianfeng, Baoguo Chen, and Lisa X. Xu. "Shear Stress Effect on the Production of Nitric Oxide in Cultured Rat Aorta Endothelial Cells." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-33074.

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Atherosclerotic lesions tend to develop in regions where there are separations from unidirectional laminar blood flow, typically near branches, bifurcations, regions of arterial narrowing, and curvatures in the arteries (1, 2). Obviously, homodynamic forces play a key role in atherosclerosis. Studies also indicate that vascular endothelium function disturbance, especially impairment of endothelium dependent vasodilation, is involved (3). Shear stress affects endothelial cells in many ways, such as cytoskeletal rearrangement, decrease of intracellular pH, release of PGI2 and some growth factors (PDGF, FGF, ECGF, TGF-b, etc), activation of IP3 and mitogen-activated protein kinases, and the significant increase in the production of nitric oxide (1,2,4,5). As an important function factor of vascular endothelial cells, nitric oxide (NO) is closely related to the endothelial dysfunction and atherosclerosis (6). Endothelial derived nitric oxide involves in many events in the vasculature, including vasodilation, inhibition of platelet aggregation, adhesion molecule expression, and vascular smooth muscle proliferation, which are directly or indirectly related to atherosclerosis. Endothelial cells release NO more potently in response to increased shear stress than to agonists that raise intracellular free calcium concentration [Ca2+]i. Studies have indicated that NO production increases with a calcium/CaM dependent manner in the first few minutes after exposed to shear stress, followed by a sustained NO production that occurs more than 30min which is Ca2+ independent (7). The activation of eNOS by shear stress, which modulated by Ca/CaM, G protein, tyrosine kinase phosphorylation and eNOS gene expression, is responsible for the increase of NO production (8). However, the contribution of extracellular calcium to the production of NO is somewhat contradictory.

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Scrobohaci, M. L., L. Drouet, B. Baudin, and A. Rodriguez. "DIFFERENTIAL CHANGESOF PLASMATIC MARKERS OF THE ENDOTHELIAL FOLLOWING dDAVP." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644134.

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Plasmatic levels of tissue plasminogen activation is commonly assumed to be of endothelial origin ; Angiotensin converting enzyme can be of endothelial or monocytic origin;Fibronectin is mostly from hepatic origin but endothelium can participate. Protein S is a newly recognized endothelial protein. Plasmatic von Willebrand factor is mostly from endothelial origin as the factor megakaryocytic origin is stored in platelet αd granules.dDAVP by indirect effect stimulates release of endothelial factors,13 patients with moderate von Willebrand disease were submitted to an infusion of 0.4 ug/kg dDAVP and were followed for four hours after infusion.Interstingly the kinetics of release of each of the studied factors is totally different.-Tissue plasminogen activator israpidly released and come back alsoquickly to its original level,- Release of von Willebrand factor is delayed comparatively to tPA and stayed for a longer time at increased level,- Angiotensin converting enzyme is not affected by dDAVP while its level is stimulated by veno-occlusion- Fibronectin and Protein S arenot significantly modified by dDAVPFrom these results mechanism of action of dDAVP cannot be hypothesized, but it seems evident that the release (and so the endothelial metabolism) of each of the studied factorsis different and not linked.

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Klein-Soyer, C., F. Driot, J. L. Vonesch, et al. "MODULATION BY HEPARINS OR PENTOSAN POLYSULFATE OF THE EFFECTS OF ACIDIC AND BASIC HUMAN FIBROBLAST GROWTH FACTORS (aFGF and bFGF) ON THE REPAIR OF A MECHANICAL LESION OF THE ENDOTHELIUM." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643358.

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A mechanical injury to endothelium (EC) may be followed by vascular spasm, platelet adhesion to exposed subendothelium, mural thrombosis and atherosclerosis. Heparin (HEP) can protect EC from injury, inhibits smooth muscle cells proliferation and has been proposed in the treatment of atherosclerosis. aFGF and bFGF are potent mitogens for EC in vitro and angiogenic in vivo. HEP increases the growth promoting activity of aFGF in EC culture. We have studied the effects of HEP (Choay), low molecular weight HEP (LMWH, CY216 Choay) or pentosan poly sulfate (PPS, Clin-Midy) in the presence of aFGF or bFGF on the repair process, after a mechanical injury of confluent cultured human EC by application of a 6 mm diameter cellulose polyacetate paper. Time for 50 % regeneration (T50) of the lesion was calculated after measuring the remaining lesion at time intervals. Human aFGF (brain) and bFGF (placenta) were purified by HPLC and identified by N-terminus analysis. They were used at concentrations that did not modify T50 when added to 5 % serum. HEP, LMWH and PPS (100 μg/ml) alone increased T50. Addition of HEP, LMWH, or PPS to aFGF markedly decreased T50. This effect was not present with bFGF, although their inhibitory effect alone was abolished. The FGFs alone or in the presence of HEP produce an increase in EC density. In this model, the repair of the EC lesion involves cell migration and proliferation and responds to the combined action of FGFs and HEP, LMWH or PPS. Thus, these drugs could be used to stimulate the repair of injured EC and prevent blood-vessel wall interactions leading to thrombosis or atherosclerosis.

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Wingate, Kathryn, Yan Tan, Raphael Nemenoff, and Wei Tan. "Combined Effects of Nanofiber Matrix Elasticity and VEGF-A on the Differentiation of Mesenchymal Stem Cells Towards Mature Endothelial Cells." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80747.

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The potential of mesenchymal stem cell (MSC) in the treatment of vascular diseases is becoming increasingly recognized.[1] The use of MSC to produce a functional endothelium in synthetic vascular grafts is of particular interest as this would prevent common graft failures such as neointima hyperplasia and thrombus. Current attempts to produce a functional endothelial layer with endothelial cells (EC) have limited success due to the need for invasive surgery and the limited expansion capability these cells have in vitro.[2] MSC are a powerful cellular alternative as they are easily obtained through a bone marrow biopsy, have a large expansion capability in vitro, are multipotent, and thromboresistant. Individual factors such as matrix elasticity, matrix structure, growth factors, and mechanical stimulations have all been shown to contribute to MSC differentiation towards vascular phenotypes in vivo. However, the response of MSCs to the combined effects of these factors is not well characterized. Additionally, many experiments studying MSC differentiation are conducted on 2D substrates instead of simulating the 3D nanofiber matrix structure found in-vivo. Furthermore, little is known about the underlying cell signaling pathways that direct vascular differentiation. Currently, researchers have yet to achieve MSC differentiation into mature, functional endothelial cells, a critical step for regenerating healthy vascular tissue. We hypothesize that the combined effects of VEGF-A growth factor and a 3D matrix elasticity that mimicking the mechanochemical properties of in-vivo intima induce more complete MSC differentiation into EC expressing mature markers through the regulation of critical vascular signaling molecules such as MAPK/ERK and RhoA/Rock.

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