Journal articles on the topic 'Endothelium'
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1
Cardell, LO, R. Uddman, and L. Edvinsson. "Endothelins: A Role in Cerebrovascular Disease?" Cephalalgia 14, no. 4 (August 1994): 259–65. http://dx.doi.org/10.1046/j.1468-2982.1994.1404259.x.
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Vasoactive factors produced and released by the endothelium exert a powerful influence on vascular tone in the cerebral circulation. Impaired endothelium-dependent responses, such as decreased production of endothelium-derived relaxing factors, and/or release of endothelium-derived contractile factors may give rise to different pathophysiological conditions. Among the endothelium-derived contractile factors the endothelins have recently received particular attention. Endothelin-1 is the major isoform in the endothelin family, which also includes endothelin-2 and endothelin-3. Endothelin-1 is synthesized within the endothelium of cerebral vessels, whereas both endothelin-1 and endothelin-3 in addition have been identified in neurons and glia. Recent electrophysiological work has suggested a neuromodulatory role for these peptides, but at present the general interest is mainly focused on their vasoactive role. Physiological stimuli such as hypoxia, anoxia, and hemodynamic shear stress will stimulate the endothelial endothelin production. In the brain, at least two types of specific subreceptors have been cloned; ETA receptors, exclusively associated with blood vessels and ETB receptors also found on glial, epithelial, and ependymal cells. The endothelins seem so far to be the most potent vasoconstrictors yet identified. The circulating plasma levels of immunoreactive endothelin are low. Since more than 80% of the total amount released from endothelial cells seems to be secreted towards the underlying smooth muscle, endothelins have been ascribed a local vasoregulatory role. Endothelins are believed to be involved in several of our most common cerebrovascular diseases and the present review comments on their possible pathophysiological role in subarachnoid haemorrhage, cerebral ischemia, and migraine.
2
Luscher, TF, and Y. Dohi. "Endothelium-Derived Relaxing Factor and Endothelin in Hypertension." Physiology 7, no. 3 (June 1, 1992): 120–23. http://dx.doi.org/10.1152/physiologyonline.1992.7.3.120.
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In resistance arteries, endothelium-derived nitric oxide inhibits vasoconstrictors;this and endothelium-dependent relaxations to acetylcholine are blunted in hypertension. The sensitivity of hypertensive resistance arteries with endothelium to intraluminal endothelin-1 is normal but is reduced without endothelium. Thus hypertension impairs endothelial regulation of the resistance circulation.
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Saenz de Tejada, I., M. P. Carson, A. de las Morenas, I. Goldstein, and A. M. Traish. "Endothelin: localization, synthesis, activity, and receptor types in human penile corpus cavernosum." American Journal of Physiology-Heart and Circulatory Physiology 261, no. 4 (October 1, 1991): H1078—H1085. http://dx.doi.org/10.1152/ajpheart.1991.261.4.h1078.
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The localization, synthesis, and activity of endothelin and the receptor types mediating its effects in penile corpus cavernosum were investigated in whole tissue and in cultured cells derived from this tissue. With immunocytochemistry, utilizing an antiendothelin 1 (ET-1) monoclonal antibody, endothelin-like immunoreactivity was localized intensely in the endothelium and to a lesser degree in the trabecular smooth muscle. Human corpus cavernosum endothelial cells in culture expressed preproendothelin 1 mRNA, as determined by Northern blot analysis. Significant amounts of endothelin-like immunoreactivity were measured by radioimmunoassay in the supernatants of corpus cavernosum endothelial cells in culture. Endothelins are potent constrictors and caused long-lasting contractions of corporeal strips in organ chambers. Equilibrium binding analysis of endothelins to their receptor sites revealed high-affinity, specific, and saturable binding of labeled endothelins to corporeal membranes. Competition binding experiments demonstrated receptors with high affinity for ET-1 and -2 and low affinity for ET-3 and another, less abundant, set of receptors with high affinity for ET-1, -2, and -3. Affinity labeling of endothelins to corporeal membranes, followed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis, revealed that ET-1 and -2 cross-linked specifically to three different molecular mass components (75, 52, and 34 kDa). ET-3 bound only to the 34-kDa component. It is concluded that human corpus cavernosum endothelium has the ability to synthesize and release endothelin, that endothelins contract corporeal smooth muscle, and that at least two distinct endothelin receptors may exist and are differentiated by their affinity for ET-3.
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Wang, Xuemei, Yanlin Zhong, Minghui Liang, Zhirong Lin, Huping Wu, and Cheng Li. "Crosslinking-Induced Corneal Endothelium Dysfunction and Its Protection by Topical Ripasudil Treatment." Disease Markers 2022 (January 13, 2022): 1–12. http://dx.doi.org/10.1155/2022/5179247.
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Purpose. To investigate the changes of corneal endothelium under different crosslinking conditions and the protective effect of ripasudil. Methods. Corneal crosslinking groups were infiltrated with riboflavin and subsequently irradiated with 0.54 J/cm2 or 1.08 J/cm2 UVA, while noncrosslinking groups included neither UVA nor riboflavin treatment, only 1.08 J/cm2 UVA and only riboflavin treatment. Corneal opacity, variations in corneal endothelial cells, and corneal thickness of all groups were observed by slit lamp, in vivo confocal microscopy, and optical coherence tomography. Immunofluorescence staining and scanning electron microscopy were performed to evaluate changes in the structure and function of the corneal endothelium. The mice that received a corneal crosslinking dose of 1.08 J/cm2 were instilled with ripasudil to explore its protective effect on the corneal endothelium. Results. Treatment with UVA and riboflavin caused an increase in corneal opacity and corneal thickness and decreased endothelial cell density. Furthermore, treatment with UVA and riboflavin caused endothelial cell DNA damage and destroyed the tight junction and pump function of the endothelium, while riboflavin or the same dose of UVA alone did not affect the endothelium. Ripasudil reduced DNA damage in endothelial cells, increased the density of cells, and protected the endothelium’s integrity and function. Conclusion. Riboflavin combined with UVA can damage the corneal endothelium’s normal functioning. The corneal endothelium’s wound healing is dose-dependent, and the ROCK inhibitor ripasudil maintains the endothelium’s pump and barrier functions.
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Xiao, Hongbo, Jun Fang, Xiangyang Lu, Zhikui Liu, Xiaojun Chen, Jinhui Liu, Jianming Su, Jine Yi, and Zhiliang Sun. "Protective effect of soluble fiber from Undaria pinnatifida on vascular endothelium in hypercholesterolemic rabbits." Canadian Journal of Animal Science 89, no. 3 (September 1, 2009): 361–67. http://dx.doi.org/10.4141/cjas08132.
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Dietary fiber could improve endothelial function and abnormal production of nitric oxide (NO) and elevated endothelin-1 (ET-1) concentration induce endothelial dysfunction. In the present study, we tested the effect of soluble fiber extracted from Undaria pinnatifida (UP) on endothelial function and NO and ET-1 production in hypercholesterolemic rabbits. After treatment with UP soluble fiber (5 or 10%) for 8 wk, endothelium-dependent vasorelaxation in isolated aortic rings, the concentrations of NO and ET-1 and malondialdehyde (MDA), and the expression of endothelial NO synthase (eNOS) gene were measured. The UP soluble fiber (5 or 10%) treatment significantly attenuated the impairment of endothelium-dependent vasorelaxation concomitantly with increase of plasma NO concentration and expression of aortic endothelial nitric oxide synthase (eNOS), reduction of plasma MDA level and ET-1 concentration and aortic ET-1 concentration. The present study indicates that the protective effects of UP soluble fiber on endothelium-mediated vasorelaxation may be related to an improved NO production and a reduced ET-1 concentration in hypercholesterolemic rabbits.Key words: Undaria pinnatifida, soluble fiber, endothelium, nitric oxide, endothelin-1, rabbit
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Tanner, Felix C., Marcel R. Tschudi, and Thomas F. Lüscher. "Endothelium, lipoproteins and atherosclerotic vascular disease." Vascular Medicine Review vmr-2, no. 2 (September 1991): 161–76. http://dx.doi.org/10.1177/1358836x9100200207.
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The endothelium modulates vascular tone by releasing nitric oxide, which is a potent vasodilator and inhibitor of platelet aggregation. Together with prostacyclin, the endogenous nitrate nitric oxide has an important protective role in preventing vasospasm and thrombus formation. In addition, the endothelium is a source of contracting factors such as endothelin-1, thromboxane A2 and endoperoxides. Due to its strategic anatomical position, the endothelium is a primary target for injurious stimuli and cardiovascular risk factors. Low density lipoproteins reduce endothelium-dependent relaxation and enhance endothelium- dependent contraction. The same pattern of endothelial dysfunction occurs in hypercholesterolaemia and atherosclerosis. These alterations of endothelial function may contribute to vasospasm, ischaemia and thrombus formation, which are common events in patients with atherosclerotic vascular disease.
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Marsden, P. A., M. S. Goligorsky, and B. M. Brenner. "Endothelial cell biology in relation to current concepts of vessel wall structure and function." Journal of the American Society of Nephrology 1, no. 7 (January 1991): 931–48. http://dx.doi.org/10.1681/asn.v17931.
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Vascular endothelium is now appreciated to modulate vessel wall structure and function in health and disease. Strategically located between the intravascular space and vessel wall proper, the endothelium has a broad capacity to modify the functional state of adjacent or trafficking cells. Furthermore, recent findings indicate that the endothelium is an interactive tissue capable of responding to numerous mechanical, chemical, and cellular stimuli. The focus of this review will be a discussion of endothelial cell biology in relation to vascular structure and function, with particular emphasis on endothelial modulation of vasomotor tone. It is evident that endothelial cells contribute to the local control of vascular tone by releasing potent vasodilatory mediators, such as endothelium-derived relaxing factor, and vasoconstrictor mediators such as endothelin-1. The endothelium also serves to modify blood-borne signals to which vascular tissues respond. The kidney shares, directly and indirectly, in these events, making this emerging new area a focus of major interest for nephrologists.
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Yang, Qingliang, Harshani Wijerathne, Jordan C. Langston, Mohammad F. Kiani, and Laurie E. Kilpatrick. "Emerging Approaches to Understanding Microvascular Endothelial Heterogeneity: A Roadmap for Developing Anti-Inflammatory Therapeutics." International Journal of Molecular Sciences 22, no. 15 (July 21, 2021): 7770. http://dx.doi.org/10.3390/ijms22157770.
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The endothelium is the inner layer of all blood vessels and it regulates hemostasis. It also plays an active role in the regulation of the systemic inflammatory response. Systemic inflammatory disease often results in alterations in vascular endothelium barrier function, increased permeability, excessive leukocyte trafficking, and reactive oxygen species production, leading to organ damage. Therapeutics targeting endothelium inflammation are urgently needed, but strong concerns regarding the level of phenotypic heterogeneity of microvascular endothelial cells between different organs and species have been expressed. Microvascular endothelial cell heterogeneity in different organs and organ-specific variations in endothelial cell structure and function are regulated by intrinsic signals that are differentially expressed across organs and species; a result of this is that neutrophil recruitment to discrete organs may be regulated differently. In this review, we will discuss the morphological and functional variations in differently originated microvascular endothelia and discuss how these variances affect systemic function in response to inflammation. We will review emerging in vivo and in vitro models and techniques, including microphysiological devices, proteomics, and RNA sequencing used to study the cellular and molecular heterogeneity of endothelia from different organs. A better understanding of microvascular endothelial cell heterogeneity will provide a roadmap for developing novel therapeutics to target the endothelium.
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Ricard, Nicolas, Rizaldy P. Scott, Carmen J. Booth, Heino Velazquez, Nicholas A. Cilfone, Javier L. Baylon, Jeffrey R. Gulcher, Susan E. Quaggin, Thomas W. Chittenden, and Michael Simons. "Endothelial ERK1/2 signaling maintains integrity of the quiescent endothelium." Journal of Experimental Medicine 216, no. 8 (June 13, 2019): 1874–90. http://dx.doi.org/10.1084/jem.20182151.
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To define the role of ERK1/2 signaling in the quiescent endothelium, we induced endothelial Erk2 knockout in adult Erk1−/− mice. This resulted in a rapid onset of hypertension, a decrease in eNOS expression, and an increase in endothelin-1 plasma levels, with all mice dying within 5 wk. Immunostaining and endothelial fate mapping showed a robust increase in TGFβ signaling leading to widespread endothelial-to-mesenchymal transition (EndMT). Fibrosis affecting the cardiac conduction system was responsible for the universal lethality in these mice. Other findings included renal endotheliosis, loss of fenestrated endothelia in endocrine organs, and hemorrhages. An ensemble computational intelligence strategy, comprising deep learning and probabilistic programing of RNA-seq data, causally linked the loss of ERK1/2 in HUVECs in vitro to activation of TGFβ signaling, EndMT, suppression of eNOS, and induction of endothelin-1 expression. All in silico predictions were verified in vitro and in vivo. In summary, these data establish the key role played by ERK1/2 signaling in the maintenance of vascular normalcy.
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Auguet, Michel, Sylvie Delaflotte, Pierre-Etienne Chabrier, and Pierre Braquet. "Characterization of endothelin receptors mediating contraction and relaxation in rabbit saphenous artery and vein." Canadian Journal of Physiology and Pharmacology 71, no. 10-11 (October 1, 1993): 818–23. http://dx.doi.org/10.1139/y93-122.
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The endothelin receptors in rabbit isolated rings of saphenous artery and saphenous vein have been characterized using endothelin-1, endothelin-2, endothelin-3, sarafotoxin S6c, and BQ123. Although artery rings were more sensitive than those from vein to the contractile action of phenylephrine, endothelin-1 was about three times more potent as a contractile agonist on vein than on artery. In rings precontracted with phenylephrine, carbachol was 10 times more potent in vein than in artery rings to induce endothelium-dependent relaxation. However, in rings precontracted to a similar tone by endothelin-1, the relaxation elicited by carbachol was reduced in the vein but remained unchanged in the artery. In endothelium-denuded saphenous artery, endothelin-1 and endothelin-2 elicited contraction with equal potency, whereas endothelin-3 and sarafotoxin S6c were weak agonists. In saphenous vein, the rank order of sensitivity was sarafotoxin S6c > endothelin-2 > endothelin-1 = endothelin-3, whereas sarafotoxin S6c and, to a lesser extent, endothelin-3 act as partial agonists. The ETA receptor antagonist BQ123 shifted, to the right, the concentration–response curves of endothelin-1 on endothelium-denuded saphenous artery (pA2 = 7.25). In the endothelium-denuded saphenous vein, 10 μM BQ123 shifted to the right only the response to high concentrations of endothelin-1. In vein but not in artery, endothelin-1 and sarafotoxin S6c induced an endothelium-dependent relaxation, which was increased, in the case of endothelin-1, in the presence of BQ123. These results indicate that the rabbit saphenous vein contains a mixed population of ETA and ETB vasoconstrictor receptors located in the smooth muscle cells and vasorelaxant ETB receptors situated on endothelial cells. In contrast, the saphenous artery only possesses smooth muscle cell ETA receptors responsible for constriction.Key words: endothelium, endothelin, vein, artery, BQ123.
11
Little, Peter J., Christopher D. Askew, Suowen Xu, and Danielle Kamato. "Endothelial Dysfunction and Cardiovascular Disease: History and Analysis of the Clinical Utility of the Relationship." Biomedicines 9, no. 6 (June 20, 2021): 699. http://dx.doi.org/10.3390/biomedicines9060699.
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The endothelium is the single-cell monolayer that lines the entire vasculature. The endothelium has a barrier function to separate blood from organs and tissues but also has an increasingly appreciated role in anti-coagulation, vascular senescence, endocrine secretion, suppression of inflammation and beyond. In modern times, endothelial cells have been identified as the source of major endocrine and vaso-regulatory factors principally the dissolved lipophilic vosodilating gas, nitric oxide and the potent vascular constricting G protein receptor agonists, the peptide endothelin. The role of the endothelium can be conveniently conceptualized. Continued investigations of the mechanism of endothelial dysfunction will lead to novel therapies for cardiovascular disease. In this review, we discuss the impact of endothelial dysfunction on cardiovascular disease and assess the clinical relevance of endothelial dysfunction.
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O'Donnell, M. P., and F. F. Vargas. "Electrical conductivity and its use in estimating an equivalent pore size for arterial endothelium." American Journal of Physiology-Heart and Circulatory Physiology 250, no. 1 (January 1, 1986): H16—H21. http://dx.doi.org/10.1152/ajpheart.1986.250.1.h16.
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Transport characteristics of capillary endothelia have been studied in numerous preparations. Little is known, however, regarding transport across the ultrastructurally similar arterial endothelium. The present studies describe a method for determining endothelial electrical resistance in the isolated, Ringer-perfused rabbit aorta. By use of silver-silver chloride electrodes, total resistance (RT) of the vessel wall was found to be 18.4 +/- 6.5 omega . cm2 (mean +/- SD; n = 10) in response to transmural passage of constant current pulses. After detergent removal of the endothelium, outer layer resistance (Rol) was 8.7 +/- 5.1 omega . cm2. Endothelial resistance (Re) was calculated to be 9.7 +/- 4.1 omega . cm2, since RT = Rol + Re. Combination of Re with previously measured hydraulic conductivity of this endothelium yielded an equivalent endothelial pore radius of 85 A, whereas a fractional pore area of 6.5 X 10(-4) was estimated from conductivity data. An alternative analysis demonstrated an endothelial slit width of 102 A. Re is similar to electrical resistances of leaky epithelia, frog mesenteric capillary, and frog muscle capillary, suggesting similar permeability characteristics in both arterial and capillary endothelia.
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Westerweel, Peter E., and Marianne C. Verhaar. "Protective Actions of PPAR-γActivation in Renal Endothelium." PPAR Research 2008 (2008): 1–9. http://dx.doi.org/10.1155/2008/635680.
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Renal endothelial damage is pivotal in the initiation and progression of renal disease. Damaged renal endothelium may be regenerated through proliferation of local endothelium and circulation-derived endothelial progenitor cells. Activation of the PPAR-γ-receptors present on endothelial cells affects their cellular behavior. Proliferation, apoptosis, migration, and angiogenesis by endothelial cells are modulated, but may involve both stimulation and inhibition depending on the specific circumstances. PPAR-γ-receptor activation stimulates the production of nitric oxide, C-type natriuretic peptide, and superoxide dismutase, while endothelin-1 production is inhibited. Together, they augment endothelial function, resulting in blood pressure lowering and direct renoprotective effects. The presentation of adhesion molecules and release of cytokines recruiting inflammatory cells are inhibited by PPAR-γ-agonism. Finally, PPAR-γ-receptors are also found on endothelial progenitor cells and PPAR-γ-agonists stimulate progenitor-mediated endothelial repair. Together, the stimulatory effects of PPAR-γ-agonism on endothelium make an important contribution to the beneficial actions of PPAR-γ-agonists on renal disease.
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Lew, R. A., and A. J. Baertschi. "Endothelium-dependent ANF secretion in vitro." American Journal of Physiology-Heart and Circulatory Physiology 263, no. 4 (October 1, 1992): H1071—H1077. http://dx.doi.org/10.1152/ajpheart.1992.263.4.h1071.
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Coculture of endothelial cells with atrial cells (R. A. Lew and A. J. Baertschi. Biochem. Biophys. Res. Commun. 163: 701-709, 1989) increased atrial natriuretic factor (ANF) release to 205 +/- 15% (n = 33 experiments) of basal secretion (2.02 +/- 0.33 ng/ml). Stimulation of ANF release by endothelial cells was significantly reduced (P < 0.05) by addition of the calcium channel antagonist nicardipine (Nic, 100 nM; by 69 +/- 4%), the guanylate cyclase activator sodium nitroprusside (SNP, 1 microM; by 97 +/- 27%), or acetylcholine (ACh, 10 microM; by 55 +/- 13%). Endothelial cell-conditioned medium elicited a 62 +/- 10% (n = 10) increase in ANF release. Rat and porcine endothelin (0.1-100 nM) each elicited a dose-dependent increase in ANF release [up to 84 +/- 14% (n = 18) over baseline]. The activity of conditioned medium was not affected by heat or trypsin treatment, but was significantly reduced by addition of Nic or SNP and was attenuated by ACh. Stimulation of ANF by 1 nM synthetic rat or porcine endothelin was also unaffected by heat or trypsin but was significantly reduced by Nic, SNP, and ACh. Addition of endothelin-specific antiserum abolished the ANF stimulatory activity of endothelial cell-conditioned medium. Neither inhibition of superoxide anion by superoxide dismutase nor inhibition of endothelium-derived nitric oxide production by NG-monomethyl-L-arginine affected the ANF release from coculture. Thus endothelial cells release a heat-stable, diffusible ANF stimulatory factor, which is not endothelium-derived relaxing factor or superoxide anion but is biologically and immunologically similar to endothelin.
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Woodman, Owen L. "Approaches to the Prevention of Coronary Vascular Dysfunction Caused by Myocardial Ischaemia and Reperfusion." Current Pharmaceutical Design 5, no. 12 (December 1999): 1077–87. http://dx.doi.org/10.2174/1381612805666230112214526.
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The endothelium is an important regulator of coronary vascular tone due to its ability to release potent vasoactive substances such as the vasodilators nitric oxide (NO), endothelium-derived hyperpolarizing factor (EDHF), prostacyclin (PGl2) and the potent vasoconstrictor endothelin. Endothelial dysfunction has been associated with a number of pathological states such as atherosclerosis, hypertension, diabetes and congestive heart failure. A disturbance of endothelial function may also contribute to the adverse effects that ischaemia and reperfusion exerts on the coronary vasculature. After ischaemia and reperfusion there is usually a selective impairment of endothelium-dependent relaxation in isolated coronary arteries. However, in the intact coronary circulation, there is a general loss of vasodilator reserve as responses to both endothelium-dependent and endothelium-independent agonists are attenuated. The release of vasoconstrictor(s) and plugging of capillaries with leukocytes may contribute to that impairment of the capacity of the coronary circulation to dilate together with the reduction in basal blood flow (no-reflow phenomenon). Ischaemic preconditioning is able to prevent ischaemic damage to the myocardium but the vasculature is less well protected as reperfusion is enhanced but the vasodilator reserve continues to be limited. Pharmacological preservation of vascular function has proved more successful with inhibitors of leukocyte adhesion, calcium channel blockers, endothelin receptor antagonists and inhibitors of oxygen radical generation all offering protection. Further refinement of protocols to preserve endothelial and vascular function after ischaemia will aid reperfusion, enhance vasodilator reserve and maximise recovery of myocardial function.
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Mebazaa, A., E. Mayoux, K. Maeda, L. D. Martin, E. G. Lakatta, J. L. Robotham, and A. M. Shah. "Paracrine effects of endocardial endothelial cells on myocyte contraction mediated via endothelin." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 5 (November 1, 1993): H1841—H1846. http://dx.doi.org/10.1152/ajpheart.1993.265.5.h1841.
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Endocardial endothelium is reported to modulate myocardial contraction by releasing diffusible factors, but the nature of the agent(s) responsible is unknown. In the present study we investigated the potential role of endothelin in these effects. Cultured sheep endocardial endothelial cells were found to express endothelin-1 mRNA and to release endothelin-1 into superfusing solution. This superfusate induced positive inotropic effects in isolated rat cardiac myocytes, associated with an increase in the cytosolic Ca2+ transient. Similar positive inotropic effects were induced by vascular endothelial cell superfusate as well as by synthesized endothelin-1, administered at concentrations similar to those present in the superfusate. Incubation of endocardial endothelial cell superfusate with endothelin-1-specific antiserum reduced the free endothelin-1 concentration to undetectable levels and abolished both the positive inotropic effect and the rise in cytosolic Ca2+. These findings indicate that endocardial endothelial cells may modulate myocardial contraction in part through the release of endothelin-1 and suggest that endocardial as well as vascular endothelium could exert potent paracrine effects on myocardium.
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Tyagi, Suresh C., Lane M. Smiley, and Vibhas S. Mujumdar. "Homocyst(e)ine impairs endocardial endothelial function." Canadian Journal of Physiology and Pharmacology 77, no. 12 (November 15, 1999): 950–57. http://dx.doi.org/10.1139/y99-102.
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Homocyst(e)ine injured vascular endothelium and modulated endothelial-dependent vascular function. Endothelium plays an analogous role in both the vessel and the endocardium. Therefore, we hypothesized that homocyst(e)ine modulated endocardial endothelium (EE) dependent cardiac function. The ex vivo cardiac rings from normal male Wistar-Kyoto rats were prepared. The contractile responses of left and right ventricular rings were measured in an isometric myobath, using different concentrations of CaCl2. The response was higher in the left ventricle than right ventricle and was elevated in endocardium without endothelium. The half effective concentration (EC50) and maximum tension generated by homocyst(e)ine were 106 and 5-fold lower than endothelin (ET) and angiotensin II (AII), respectively. However, in endothelial-denuded endocardium, homocyst(e)ine response was significantly increased (p < 0.005, compared with intact endothelium) and equal to the response to ET and AII. To determine the physiological significance of ET, AII, homocyst(e)ine, and endothelial nitric oxide in EE function, cardiac rings were pretreated with AII (10-10 M) or ET (10-13 M) and then treated with homocyst(e)ine (10-8 M). Results suggested that at these concentrations AII, ET, or homocyst(e)ine alone had no effect on cardiac contraction. However, in the presence of 10-10 M AII or 10-13 M ET, the cardiac contraction to homocyst(e)ine (10-8 M) was significantly enhanced (p < 0.01, compared with without pretreatment) and further increased in the endocardium without endothelium. The pretreatment of cardiac ring with the inhibitor of nitric oxide, Nω-nitro-L-arginine methyl ester (L-NAME), increased contractile response to homocyst(e)ine. These results suggested that homocyst(e)ine impaired EE-dependent cardiac function and acted synergistically with AII and ET in enhancing the cardiac contraction.Key words: endocardial remodeling, homocyst(e)ine, contraction, endothelin, angiotensin, endothelial-derived relaxing factor (EDRF), Nω-nitro-L-arginine methyl ester (L-NAME), endothelial dysfunction, ex vivo cardiac function, heart failure.
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Han, Jonathan, Nathan Wright, Sydni K. Davis Farhat, Florencia Yeh, and Robert E. Fintelmann. "Postcataract surgery gray-white lines of the corneal endothelium viewed with confocal microscopy and review of literature." Journal of Cataract & Refractive Surgery Online Case Reports 12, no. 2 (April 2024): e00120. http://dx.doi.org/10.1097/j.jcro.0000000000000120.
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Introduction: Cataract surgery rarely causes 1-day postoperative corneal endothelial changes visibly seen as patches or linear streaks. Previously described as “snailtracks,” these changes have been studied using slitlamp examination (SLE), scanning electron microscopy, and specular microscopy, but to the best of the authors' knowledge, it has yet to be analyzed using confocal microscopy. Patient and Clinical Findings: 3 patients who underwent cataract surgery through phacoemulsification with intraocular lens implant were found to have snailtracks on the corneal endothelium during postoperative day 1 examination. Diagnosis, Intervention, and Outcomes: The corneal endothelium of the 3 identified patients underwent SLE and in vivo confocal microscopy on postoperative day 1 and postoperative week 1. On day 1, linear opacities were visible on the corneal endothelia and confocal microscopy revealed disruptions of the regular polygonal endothelial pattern with cell aggregation. At 1 week, opacities had resolved and confocal microscopy demonstrated reorganization of the endothelia and appearance of hyperreflective nuclei. Conclusions: Confocal microscopy of postcataract surgery snailtracks supports the hypothesis that such endothelial opacification is secondary to trauma to the endothelium.
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Cameron, IT, and AP Davenport. "Endothelins in reproduction." Reproductive Medicine Review 1, no. 1 (March 1992): 99–113. http://dx.doi.org/10.1017/s0962279900000466.
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Endothelin-1 (ET-1) is a 21 amino acid peptide, first isolated in 1988 from porcine aortic endothelial cells in tissue culture (Figure 1). The peptide was shown to be the most potent known vasoconstrictor of porcine coronary arteries. A powerful endothelium-derived vasoconstrictor had been predicted for some time, but it was when Yanagisawa and his colleagues elucidated the structure, and provided information about the molecular biology and mode of action of the peptide that an unprecedented interest was stimulated in the endothelins.
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Gavrilova, Natalya Alexandrovna, and Olga Evgen'evna Tishchenko. "Vliyanie sulodeksida na funktsional'noe sostoyanie endoteliya u bol'nykh s sakharnym diabetom i diabeticheskoyretinopatiey." Diabetes mellitus 14, no. 2 (June 15, 2011): 66–68. http://dx.doi.org/10.14341/2072-0351-5637.
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Aim. To study effect of sulodexide (Vessel Due F) on the functional state of endothelium in patients with diabetic retinopathy. Materials and methods. A total of 37 patients with DR were divided in 2 groups and treated with sulodexide. Group 1 comprised 16 patients withnon-proliferative DR, group 2 included 21 patients with preproliferative DR. The functional state of endothelium was estimated from the plasma andserum levels of endothelial factors (sVCAM, endothelin, nitric oxide, t-PA, Willebrand factor). Results. The measurement of the initial levels of endothelial factors in both groups revealed significant changes in endothelin, nitric oxide, and sVCAMsuggesting disturbances of endothelial function due to DR. Sulodexide therapy normalized it regardless of DR stage and thereby improved functionalactivity of retina. Conclusion. This study has demonstrated beneficial effect of sulodexide on endothelial function in patients with DR due to correction of the productionof vasoactive factors (endothelin, nitric oxide) and stimulation of fibrinolytic activity of the vascular wall (t-PA).
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Gaine, Sean P., Mariesa A. Hales, and Nicholas A. Flavahan. "Hypoxic pulmonary endothelial cells release a diffusible contractile factor distinct from endothelin." American Journal of Physiology-Lung Cellular and Molecular Physiology 274, no. 4 (April 1, 1998): L657—L664. http://dx.doi.org/10.1152/ajplung.1998.274.4.l657.
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Hypoxia (0% O2) evokes a late-phase, endothelium-dependent contractile response in porcine isolated pulmonary arteries that may be caused by a cyclooxygenase-independent, endothelium-derived contractile factor. The aim of this study was to further analyze the mechanism underlying this hypoxic response. Proximal porcine pulmonary arterial rings were suspended for isometric tension recording in organ chambers. Hypoxia (0% O2) caused a late-phase, endothelium-dependent contractile response that was not inhibited by the endothelin (ET)A-receptor antagonist BQ-123 (10−6 M), by the ETB-receptor antagonist BQ-788 (10−7 M), or by their combination. In contrast, ET-1 caused a concentration-dependent contraction of arterial rings that was inhibited by BQ-123 (10−6 M) and a relaxation that was abolished by BQ-788 (10−7 M) or by endothelial cell removal. Therefore, the endothelium-dependent contraction to hypoxia is not mediated by ET. Hypoxia caused only relaxation in endothelium-denuded rings. However, when a pulmonary valve leaflet, a rich source of pulmonary endothelial cells, was placed into the lumen of endothelium-denuded rings, hypoxia caused a late-phase contractile response that was similar to that observed in arterial rings with native endothelium. This hypoxic contraction persisted in the presence of indomethacin (10−5 M) and N-nitro-l-arginine methyl ester (3 × 10−5M) to block cyclooxygenase and nitric oxide synthase, respectively. These results suggest that hypoxic contraction of pulmonary arteries is mediated by a diffusible, contractile factor released from hypoxic endothelial cells. This contractile mediator is distinct from ET.
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Dilmuradova K.R and Ziyadullayeva H.O. "Study of the relationship between hemostasis and vascular endothelium in hypoxic lesions of the nervous system in newborns." Texas Journal of Medical Science 22 (July 24, 2023): 24–26. http://dx.doi.org/10.62480/tjms.2023.vol22.pp24-26.
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The study of the statement of the hemostatic system and vascular endothelium was made in newborns with hypoxic lesions of the nervous system. Some indicators of hemostasis (PTT, APTT, TT and fibrinogen) were determined in cord blood, as well as endothelial dysfunction marker Endothelin-1. In newborns who underwent a chronic hypoxia, a statistically significant increase of the fibrinogen level and endothelin-1 were revealed in the umbilical cord blood. During hypoxic lesions of the nervous system in newborns the vascular endothelium primarily reacts, causing activation of hemostasis and cerebral blood flow disorders.
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Chirila, Traian V., Peter W. Madden, and Lawrie W. Hirst. "Replacement of the Corneal Endothelium and the Conceptual Framework for an Artificial Substitute." Journal of Biomimetics, Biomaterials and Tissue Engineering 5 (February 2010): 13–29. http://dx.doi.org/10.4028/www.scientific.net/jbbte.5.13.
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Dysfunction of the corneal endothelium due to cell loss caused by aging, disease or trauma can lead to severe visual impairment and blindness. Traditionally, dysfunctional endothelia are managed surgically, by removing the entire central cornea and transplanting either donor corneal tissue (penetrating keratoplasty), or just endothelia isolated from donor corneas. As in many cases it is only the corneal endothelium requiring replacement, many attempts were made over the last decades to develop an endothelial substitute, thereby precluding the need for the use of full donor corneas. This article reviews these attempts, which include artificial membranes, cell-coated corneal transplants, and cell-coated membranes. The presumption of an artificial corneal endothelium capable of duplicating the transendothelial ion-and-fluid transport function is examined in light of the latest hypotheses regarding the mechanism of this function.
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Gutsulyuk, V., I. Savytskyi, S. Tsypoviaz, S. Znamerovskyi, V. Sarahan, and T. Gerasymenko. "Study of indicators of endothelial dysfunction in rats with experimental peritonitis." Journal of Education, Health and Sport 12, no. 1 (January 31, 2022): 514–22. http://dx.doi.org/10.12775/jehs.2022.12.01.043.
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The article presents the results of the study of the activity of endothelial and inducible NO-synthase, the level of Willebrand factor and endothelin-1 in rats with experimental peritonitis. The most likely mechanism that is damaged in the endothelium during peritonitis is the activation of the synthesis of inducible NO-synthase by neutrophils/macrophages in response to infection. It is possible that hyperproduction of nitric oxide (NO), on the one hand, is aimed at destroying microflora and oxidizing toxins, and on the other hand, at suppressing the expression of tissue factor and cell adhesion molecules. platelet aggregation and cascade disorders in the hemostasis system. All this indicates that the hyperproduction of NO not only reflects the processes that occur in the focus of damage to the vascular endothelium, but also affects the severity of the inflammatory process and the outcome of the disease. In animals with experimental peritonitis on the background of OS, an increase in the number of circulating desquamated endothelial cells in the blood, which is a highly specific marker of endothelial dysfunction, was noted. The level of the Willebrand factor also increased, which can serve as a marker of increased risk of thrombus formation and indicate the pathogenetic dependence of the factors that damage the vascular wall endothelium on the concentration of the Willebrand factor, which contributes to the reduction of vascular permeability by adhesion of platelets to the endothelium. Confirmation of the development of endothelial dysfunction in peritonitis is an increase in the concentration of endothelin-1, which is a regulator of the process of vascular neoangiogenesis in response to endothelial damage.
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Shasby, D. Michael. "Cell-cell adhesion in lung endothelium." American Journal of Physiology-Lung Cellular and Molecular Physiology 292, no. 3 (March 2007): L593—L607. http://dx.doi.org/10.1152/ajplung.00386.2006.
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Homotypic cell-cell adhesion is essential for tissue and organ development, remodeling, regeneration, and physiological function. Whereas a significant number of homotypic cell-cell adhesion molecules have been identified, much more is known about those concentrated in epithelia than in endothelia. Among the endothelial cell-cell adhesion molecules, very little is known that is specific to endothelium in the pulmonary and bronchial circulations. This review focuses primarily on homotypic cell-cell adhesion molecules that are or are likely to be important in lung endothelium.
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Nechunaeva, Ye V., G. I. Shumakher, Ye N. Vorobiyova, A. V. Timoshnikov, and M. A. Khoreva. "Immunal and biochemical indexes in early diagnostics of chronic brain ischemia." Bulletin of Siberian Medicine 10, no. 2 (April 28, 2011): 142–46. http://dx.doi.org/10.20538/1682-0363-2011-2-142-146.
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The paper presents results of clinical and laboratory investigation of 106 patients with chronic brain ischemia (CBI) I—II stages, included detection levels of circulating desquamated endothelial cells, endothelin-1, autoantibodies to encephalitogenic protein, neuron-specific enolase and protein S100. Reliable changes of immune status as well as signs of endothelium dysfunction progressed with stage of CBI. Direct correlation between intensity of endothelium dysfunction and activity of neurodegererative process in brain was revealed.
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Xuan, A. T. Dinh, and T. W. Higenbottam. "Non-Prostanoid Endothelium-Derived Vasoactive Factors." Journal of International Medical Research 17, no. 4 (July 1989): 305–15. http://dx.doi.org/10.1177/030006058901700401.
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Endothelium-derived relaxing factor (EDRF) and endothelium-de-rived contracting factor (EDCF) are released by endothelial cells following stimulation by a wide range of chemical agonists acting on specific endothelial membrane receptors and by physical factors such as shear stress on the vascular wall. It has now been firmly established that EDRF is nitric oxide, whereas EDCF has been recently identified as a 21-residue peptide, endothelin. Circumstantial evidence, however, suggests that there may be more than one EDRF and/or EDCF. EDRF induces relaxation of the underlying vascular smooth muscle by enhancing intracellular cyclic GMP levels. This action is comparable to that of nitrovasodilators, and nitric oxide can, therefore, be regarded as an endogenous nitrovasodilator. The mechanism of action of endothelin is uncertain, but depends on influx of extracellular calcium. The respective roles of EDRF and EDCF in disease are still hypothetical. It is preferable to think in terms of balance (or imbalance) between these two factors which, probably, have a fundamental role, and very likely interact with each other in maintaining and regulating vascular tone in man.
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Stockelman, Kelly A., Anthony R. Bain, Caitlin A. Dow, Kyle J. Diehl, Jared J. Greiner, Brian L. Stauffer, and Christopher A. DeSouza. "Regular aerobic exercise counteracts endothelial vasomotor dysfunction associated with insufficient sleep." American Journal of Physiology-Heart and Circulatory Physiology 320, no. 3 (March 1, 2021): H1080—H1088. http://dx.doi.org/10.1152/ajpheart.00615.2020.
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Habitual insufficient nightly sleep (<7 h/night) is associated with increased risk of cardiovascular disease and events. Endothelial dysfunction, specifically reduced endothelium-dependent vasodilation and increased endothelin (ET)-1-mediated vasoconstriction, is considered to be a major contributing mechanism underlying increased vascular risk with insufficient sleep. In contrast to insufficient sleep, regular aerobic exercise enhances endothelial vasomotor function, reducing the risk of cardiovascular disease and associated events. In the present study, we determined the effects of aerobic exercise training on endothelium-dependent vasodilation and ET-1 vasoconstriction in adults who habitually sleep <7 h/night. After exercise training, although nightly sleep duration was unchanged, endothelium-dependent vasodilation was significantly enhanced and ET-1-mediated vasoconstrictor tone was significantly reduced in adults who sleep <7 h/night. Regular aerobic exercise training can mitigate insufficient sleep-related endothelial vasomotor dysfunction and, in turn, potentially reduce the cardiovascular risk associated with habitual insufficient nightly sleep.
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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 (January 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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Hendrickx, Jan, Kris Doggen, Ellen O. Weinberg, Pascale Van Tongelen, Paul Fransen, and Gilles W. De Keulenaer. "Molecular diversity of cardiac endothelial cells in vitro and in vivo." Physiological Genomics 19, no. 2 (October 4, 2004): 198–206. http://dx.doi.org/10.1152/physiolgenomics.00143.2004.
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In addition to a number of common features, cardiovascular endothelium displays structural, functional, and genetic differences according to its position in the cardiovascular tree. In the heart, endocardial and cardiac microvascular endothelia (CMVE) interact directly with surrounding cardiomyocytes, whereas the endothelium within blood vessels interacts with smooth muscle cells. In this study, we investigated whether cardiac endothelial cells were distinct from aortic endothelial (AE) cells at the transcriptional level. Using Affymetrix microarray technology and subsequent real-time PCR analyses for validation, we identified sets of genes with marked preferential expression in cultured endocardial endothelium (EE) compared with cultured AE and vice versa. Among the genes preferentially expressed in EE, some were also expressed in cultured CMVE. Immunohistochemical staining of cardiac and aortic tissue revealed that the endothelial genetic diversity observed in culture reflects, in part, a physiological diversity existing in vivo. The identification of a set of genes preferentially expressed in EE provides new insights in the functional adaptations of this endothelial subtype to its intracavitary localization and to its role in the control of ventricular performance.
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Shilkina, N. P., I. E. Yunonin, S. V. Butusova, E. V. Mikhailova, and A. A. Vinogradov. "Endothelial damage and circadian blood pressure profile in rheumatoid arthritis." Terapevticheskii arkhiv 91, no. 5 (May 15, 2019): 89–95. http://dx.doi.org/10.26442/00403660.2019.05.000052.
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Aim. To study the influence of the state of endothelium on the daily profile of arterial pressure (AP) in patients with rheumatoid arthritis (RA). Materials and methods. In 70 RA pts carried out C-reactive protein (CRP), vascular endothelial adhesion molecule type 1 (sVCAM-1), antigen von Willebrand Factor (AG WF), interleukin-8 (Il-8), rheumatoid factor (RF), IgG, endotheline-1 (ET-1), number of desquamated endotheliocytes cells (DE), VS, activity of renin by immunoenzyme analysis. The dysfunction of endothelium was evaluated by calculation of DE. The functional methods included the daily monitoring of arterial pressure (AP). Results. Arterial hypertension (AH) occurred in 40 (57.1%) pts. RA pts are revealed the signs of endothelial dysfunction, about which significant differences among the indices of activation of endothelium in comparison with control group testify. ET-1, sVCAM-1, vWF AG, Il-8, CRP content was higher in RA pts. Reliably above there was a number of DE. Reliable differences according to these indices depending of RA activity were discovered. With conducting of correlation analysis it is revealed, that markers of the activation of endothelium: sVCAM-1, vWF AG positively correlated with increasing RF IgG and indices of the immune inflammation: CRP, and DE number. In patients suffering from RA, showed signs of endothelial dysfunction. The positive correlation between endothelial damage and daily profile of AP show the relationship of these processes. Conclusion. Positive correlations between the damage of endothelium and disturbance of AP daily profile testify about the interrelation of these processes.
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Denesyuk, V. "Advances in the Investigation of Vascular Remodeling and Endothelial Function in Heart Disease Over the Past Decades (Literature Review and Own Results)." Lviv clinical bulletin 2, no. 42 (July 23, 2023): 72–78. http://dx.doi.org/10.25040/lkv2023.02.072.
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Introduction. Studies of vascular remodeling and endothelial dysfunction induced by different cardiological pathologies are far from complete. The aim of the study. To analyze recent advances in the investigation of vascular remodeling and endothelial dysfunction on the background of cardiological diseases according to literature database and own research results. Materials and methods. Literature survey of 49 articles was supplemented with own research results. Results. By means of dopplerography it was detected brachial artery hypertrophy, which is a risk factor for myocardial infarction and stroke. Endothelium, which secretes vasoactive substances (nitric oxide – NO, endothelin-1, prostacyclin, thromboxane, etc.) plays an important role in the histophysiology of coronary arteries. Dysfunction of endothelium plays a key role in the development of atherosclerosis, coronary heart disease, hypertension, heart failure even before the appearance of clinical signs of diseases. In myocardial infarction, the development of endothelial dysfunction was detected by various methods. The predictors of an unfavorable prognosis in patients with acute myocardial infarction with elevated ST-segment include a violation of endothelium-dependent vasodilatation as revealed by test for hyperemia. Similarly, an unfavorable prognostic factor in myocardial infarction is the increased level of endothelin-1. Conclusions. In patients with arterial hypertension, coronary heart disease, unstable angina pectoris, myocardial infarction, hypertrophic remodeling of the brachial artery alongside with a decrease in endothelium-dependent vasodilatation were detected by various older and new methodes. Currently it is generally accepted that changes in arteries and disruption of endothelial function are the root cause of diseases of the heart and blood vessels. On the basis of the conducted research, correction of the detected changes is carried out, aimed at preventing the progression of diseases of the cardiovascular system. Keywords: vascular remodeling, endothelial dysfunction, heart diseases.
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King, A. J., and B. M. Brenner. "Endothelium-derived vasoactive factors and the renal vasculature." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 260, no. 4 (April 1, 1991): R653—R662. http://dx.doi.org/10.1152/ajpregu.1991.260.4.r653.
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The endothelium is now recognized to transduce intravascular hemodynamic and chemical signals into appropriate changes in vascular smooth muscle (VSM) tone. The effector branch of this transduction is due, at least in part, to endothelial release of potent soluble vasoactive mediators. Two such mediators, endothelium-derived relaxing factor (EDRF) and endothelin, have markedly different chemical composition and contrasting effects on VSM tone. EDRF, identified to be nitric oxide or a nitrosothiol, is a vasodilator, whereas endothelin, a 21-amino acid polypeptide, is the most potent vasoconstrictor yet described. Considerable evidence has been amassed to suggest that these molecules play an important role in the regulation of basal renal hemodynamics and in the pathogenesis of acute renal failure. The purpose of this editorial review is to examine the data supporting a role for the endothelium in the regulation of renal hemodynamics in normal and pathological states.
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Stepanova, T. V., A. N. Ivanov, N. E. Tereshkina, E. B. Popyhova, and D. D. Lagutina. "MARKERS OF ENDOTHELIAL DYSFUNCTION: PATHOGENETIC ROLE AND DIAGNOSTIC SIGNIFICANCE." Russian Clinical Laboratory Diagnostics 64, no. 1 (April 29, 2019): 34–41. http://dx.doi.org/10.18821/0869-2084-2019-64-1-34-41.
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Endothelial dysfunction (ED) is considered one of the pathogenetic mechanisms of a whole range of diseases. Detection of specific biochemical markers in the blood is an effective way to ED diagnostics that characterize the vascular endothelium state. This review highlights the pathogenetic role of the factors synthesized by endotheliocytes whose level changes in biological fluids reflect violations of the endothelium basic physiological properties: vasomotor function, thromboresistance, angiogenesis regulation, barrier and adhesion functions. In particular, the participation of nitric oxide metabolites, asymmetric dimethylarginine, endothelin-1, metabolic products of arachidonic acid, von Willebrand factor, thrombomodulin, vascular endothelial growth factor, vasohibine-1 and adhesion molecules in the onset and development of ED are reviewed. The diagnostic significances of factors damaging endothelium, such as C-reactive protein, homocysteine and 8-hydroxy-2’-deoxyguanosine, are discussed. In addition, the literature data of recent years about the prospects of clinical implication the detection of the above-mentioned factors which indicates structural and functional endothelial cells damage are given. Particular attention is paid to the ED markers detection prognostic significance and the possibility of their practical use for the ED diagnosis. The search of literature for the current review was conducted in RSIC, CyberLeninka, Scopus, Web of Science, MedLine and PubMed databases from 2012 to 2018 using the following keywords: endothelial dysfunction, nitric oxide, asymmetric dimethylarginine, endothelin-1, prostacyclin, thromboxane A2, epoxyeicosatrienoic acids, von Willebrand factor, thrombomodulin, vascular endothelial growth factor, vasohibin-1, adhesive molecules, C-reactive protein, homocysteine, and 8-hydroxy-2-deoxyguanosine.
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Thorin, Eric, and David J. Webb. "Endothelium-derived endothelin-1." Pflügers Archiv - European Journal of Physiology 459, no. 6 (December 5, 2009): 951–58. http://dx.doi.org/10.1007/s00424-009-0763-y.
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Nakashima, M., and P. M. Vanhoutte. "Endothelin-1 and -3 cause endothelium-dependent hyperpolarization in the rat mesenteric artery." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 6 (December 1, 1993): H2137—H2141. http://dx.doi.org/10.1152/ajpheart.1993.265.6.h2137.
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The present study was designed to determine whether endothelin (ET) induces endothelium-dependent hyperpolarization in the isolated rat mesenteric artery and, if so, to identify the receptor subtype involved. Main superior mesenteric arteries of Wistar-Kyoto and spontaneously hypertensive rats were used for the measurement of electrical responses of smooth muscle cells, using glass microelectrode. In tissues with endothelium of both strains, ET-1 (10(-8) M) caused an initial transient hyperpolarization followed by a sustained depolarization. In tissues without endothelium, only depolarization was observed. ET-3 (10(-8) M) produced transient hyperpolarizations only in preparations with endothelium. There was no significant difference in maximal amplitude of hyperpolarization between the two strains. BQ-123 (selective ETA-receptor antagonist) blocked the depolarization to ET-1 but did not inhibit hyperpolarizing responses to either isopeptide. IRL-1620 (specific ETB-receptor agonist) produced transient membrane hyperpolarizations in tissues with endothelium. The hyperpolarizations induced by ET were not affected by NG-nitro-L-arginine. These data suggest that both ET-1 and ET-3 can cause endothelium-dependent hyperpolarization in the rat mesenteric artery and that the endothelial receptor involved may belong to ETB subtype.
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Mijovic, Romana, Branislava Ilincic, Suncica Kojic-Damjanov, Biljana Vuckovic, Radmila Zeravica, and Velibor Cabarkapa. "Influence of metabolic disorders on phenotypic modulation of vascular endothelium in type 2 diabetes mellitus." Medical review 70, no. 11-12 (2017): 437–43. http://dx.doi.org/10.2298/mpns1712437m.
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Introduction. Endothelium is a dynamic, strategically positioned defensive regulator of vascular homeostasis. Physiology and Pathophysiology of Vascular Endothelium. Endothelial phenotypic modulation involves five basic characteristics: the expression of leukocyte adhesion molecules, the production of cytokines, change in the shape and the permeability of the endothelium, prothrombotic changes and upregulation of autoantigens. Obesity, Metabolic Inflammation and Vascular Endothelium One of the most important pathophysiological manifestations of adiposopathy may be the phenotypic conversion of vascular endothelium. Insulin Resistance and Vascular Endothelium. Under the conditions of insulin resistance and consequent hyperinsulinemia, there is imbalance between the production of endothelial vasoconstrictors and vasodilators, increased expression of adhesion molecules, and platelet hyperreactivity. Hyperglycemia and Vascular Endothelium. Hyperglycemia causes endothelial dysfunction by various mechanisms that involve activation of polyol pathway and production of sorbitol, increased formation of advanced glycation end products, activation of various isoforms of protein kinase C and activation of hexosamine pathway. Dyslipidemia and vascular endothelium. Dyslipidemia takes an important role in a cascade of pathophysiological processes that result in endothelial activation and chronic dysfunction. Conclusion. Hyperglycemia, hyperinsulinemia, insulin resistance, dyslipidemia, visceral obesity and low-grade inflammation are the main factors responsible for development of endothelial dysfunction in type 2 diabetes mellitus.
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Moreau, Pierre, and Ernesto L. Schiffrin. "Role of endothelins in animal models of hypertension: focus on cardiovascular protection." Canadian Journal of Physiology and Pharmacology 81, no. 6 (June 1, 2003): 511–21. http://dx.doi.org/10.1139/y03-015.
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Investigation of the regulation of vascular function by endothelium-derived factors has been a prominent topic of research in the field of hypertension during the last decade. Of the different endothelial factors, endothelins, which play an important role in vasodilatationvasoconstriction balance, have been the subject of great interest and an impressive number of publications. This peptide, a very potent vasoconstrictor, triggers as well events involved in growth, proliferation, matrix production and local inflammation. In parallel, its role in hypertension has evolved from a simple vasoconstrictor to a central local regulator of vascular homeostasis contributing not only to the elevation of blood pressure, but also to the complications of hypertension. This review summarizes research on endothelins and its receptor antagonists in experimental hypertension, with special emphasis on vascular remodeling and target-organ protection.Key words: endothelin, endothelin antagonists, hypertension, vascular remodeling, hypertrophy, target-organ damage.
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Mariassy, A. T., M. K. Glassberg, M. Salathe, F. Maguire, and A. Wanner. "Endothelial and epithelial sources of endothelin-1 in sheep bronchi." American Journal of Physiology-Lung Cellular and Molecular Physiology 270, no. 1 (January 1, 1996): L54—L61. http://dx.doi.org/10.1152/ajplung.1996.270.1.l54.
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Airway smooth muscle tone and growth is regulated by endothelin-1 (ET-1), but the sources of ET-1 in the airway wall have not been clearly defined. We therefore wished to estimate the relative contributions of the epithelium and endothelium to ET-1 production in the bronchi (mean ID 1.7-4.9 mm) of mature normal sheep. Morphometric assessment of bronchial cross-sections revealed a number of epithelial cells three times greater than endothelial cells by direct cell count. In contrast, the overall cell surface density was five to six times greater, and the airway smooth muscle-centered cell surface density was three to four times greater for endothelial cells than for epithelial cells. The expression of preproendothelin-1 mRNA was detected in cultured aortic endothelial cells (as a substitute for bronchial endothelial cells) but not in cultured bronchial epithelial cells, and the former secreted seven times more immunoreactive ET-1 than the latter. These findings show that topographically the endothelium is better positioned for the regulation of ovine bronchial smooth muscle than the epithelium. Furthermore, the findings suggest greater constitutive ET-1 secretion by cultured endothelium than by epithelium.
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CORDER, Roger, Richard C. WARBURTON, Noorafza Q. KHAN, Ruth E. BROWN, Elizabeth G. WOOD, and Delphine M. LEES. "The procyanidin-induced pseudo laminar shear stress response: a new concept for the reversal of endothelial dysfunction." Clinical Science 107, no. 5 (October 26, 2004): 513–17. http://dx.doi.org/10.1042/cs20040189.
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Reduced endothelium-dependent vasodilator responses with increased synthesis of ET-1 (endothelin-1) are characteristics of endothelial dysfunction in heart failure and are predictive of mortality. Identification of treatments that correct these abnormalities may have particular benefit for patients who become refractory to current regimens. Hawthorn preparations have a long history in the treatment of heart failure. Therefore we tested their inhibitory effects on ET-1 synthesis by cultured endothelial cells. These actions were compared with that of GSE (grape seed extract), as the vasoactive components of both these herbal remedies are mainly oligomeric flavan-3-ols called procyanidins. This showed extracts of hawthorn and grape seed were equipotent as inhibitors of ET-1 synthesis. GSE also produced a potent endothelium-dependent vasodilator response on preparations of isolated aorta. Suppression of ET-1 synthesis at the same time as induction of endothelium-dependent vasodilation is a similar response to that triggered by laminar shear stress. Based on these results and previous findings, we hypothesize that through their pharmacological properties procyanidins stimulate a pseudo laminar shear stress response in endothelial cells, which helps restore endothelial function and underlies the benefit from treatment with hawthorn extract in heart failure.
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Sabrane, Karim, Markus-N. Kruse, Alexandra Gazinski, and Michaela Kuhn. "Chronic Endothelium-Dependent Regulation of Arterial Blood Pressure by Atrial Natriuretic Peptide: Role of Nitric Oxide and Endothelin-1." Endocrinology 150, no. 5 (January 29, 2009): 2382–87. http://dx.doi.org/10.1210/en.2008-1360.
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Atrial natriuretic peptide (ANP), via its guanylyl cyclase (GC)-A receptor, plays a key role in the regulation of arterial blood pressure (ABP) and volume. Endothelial-restricted deletion of GC-A in mice [endothelial cell (EC) GC-A knockout (KO)] resulted in hypervolemic hypertension, demonstrating that the endothelium participates in the hypotensive and hypovolemic actions of ANP. Published studies showed that ANP modulates the release of the vasoactive factors nitric oxide (NO) and endothelin-1 (ET-1) from cultured endothelia. Based on these observations, we examined the role of these endothelial factors in ANP-dependent vasodilatation (studied in isolated arteries) and chronic regulation of ABP (measured in awake mice by tail-cuff plethysmography). ANP induced concentration-dependent vasorelaxations of aortic, carotid, and pulmonary arteries. These responses were not different between control and EC GC-A KO mice, and were significantly enhanced after inhibition of NO synthase [by N(G)-nitro-l-arginine-methyl ester]. Intravenous administration of N(G)-nitro-l-arginine-methyl ester to conscious mice significantly increased ABP. The extent of these hypertensive reactions was similar in EC GC-A KO mice and control littermates (increases in systolic blood pressure by ∼25 mm Hg). Conversely, antagonism of ET-1/endothelin-A receptors with BQ-123 reduced ABP significantly and comparably in both genotypes (by ∼11 mm Hg). Finally, the vascular and tissue expression levels of components of the NO system and of immunoreactive ET-1 were not different in control and EC GC-A KO mice. We conclude that the endothelium, but not modulation of endothelial NO or ET-1, participates in the chronic regulation of ABP by ANP.
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Dièye, Amadou Moctar, and Alexis Gairard. "Endothelium and aortic contraction to endothelin-1 in the pregnant rat." Canadian Journal of Physiology and Pharmacology 78, no. 5 (April 10, 2000): 372–77. http://dx.doi.org/10.1139/y99-150.
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Endothelium-derived factors modulate tone and may be involved in hyporeactivity to vasoconstrictors, such as norepinephrine or angiotensin II, as has been previously described during gestation. The endothelium produces endothelin-1, a major vasoconstrictor peptide, therefore aortic contractions to endothelin-1 (10-10 to 3 ×10-7 M) were used to assess the role of the endothelium in pregnant Wistar rats (at 20 days of gestation). Late pregnancy is characterized by a significantly diminished systolic blood pressure in conscious rats (-17 mmHg, P < 0.001, n = 14). In pregnant and in age-matched nonpregnant female rats, endothelin-1 induced aortic contraction was greater when endothelium was present (at least P < 0.01). Indomethacin significantly reduced this contraction in aortic rings with intact endothelium in all groups. In aortic rings that had endothelium physically removed, contraction to endothelin-1 was greater in pregnant rats than in nonpregnant ones. Indomethacin decreased contraction of aortic rings in pregnant rats only. These results suggest an enhanced synthesis of vasoconstrictors by cyclooxygenases in vascular smooth muscle during pregnancy. In vessels with intact endothelium, we did not find hyporeactivity to endothelin-1 during late pregnancy. Contraction to endothelin-1 involved ETA receptors because it was decreased by BQ-123, an ETA receptor antagonist, whereas there was no significant change when using BQ-788, an ETB receptor antagonist. Key words: endothelin-1, endothelium, contraction, aorta, gestation.
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Szczesny-Malysiak, Ewa, Marta Stojak, Roberto Campagna, Marek Grosicki, Marek Jamrozik, Patrycja Kaczara, and Stefan Chlopicki. "Bardoxolone Methyl Displays Detrimental Effects on Endothelial Bioenergetics, Suppresses Endothelial ET-1 Release, and Increases Endothelial Permeability in Human Microvascular Endothelium." Oxidative Medicine and Cellular Longevity 2020 (October 14, 2020): 1–16. http://dx.doi.org/10.1155/2020/4678252.
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Nrf2 is a master regulator of antioxidant cellular defence, and agents activating the Nrf2 pathway have been tested in various diseases. However, unexpected side effects of cardiovascular nature reported for bardoxolone methyl in patients with type 2 diabetes mellitus and stage 4 chronic kidney disease (the BEACON trial) still have not been fully explained. Here, we aimed to characterize the effects of bardoxolone methyl compared with other Nrf2 activators—dimethyl fumarate and L-sulforaphane—on human microvascular endothelium. Endothelial toxicity, bioenergetics, mitochondrial membrane potential, endothelin-1 (ET-1) release, endothelial permeability, Nrf2 expression, and ROS production were assessed in human microvascular endothelial cells (HMEC-1) incubated for 3 and 24 hours with 100 nM–5 μM of either bardoxolone methyl, dimethyl fumarate, or L-sulforaphane. Three-hour incubation with bardoxolone methyl (100 nM–5 μM), although not toxic to endothelial cells, significantly affected endothelial bioenergetics by decreasing mitochondrial membrane potential ( concentrations ≥ 3 μ M ), decreasing spare respiratory capacity ( concentrations ≥ 1 μ M ), and increasing proton leak ( concentrations ≥ 500 nM ), while dimethyl fumarate and L-sulforaphane did not exert such actions. Bardoxolone methyl at concentrations ≥ 3 μ M also decreased cellular viability and induced necrosis and apoptosis in the endothelium upon 24-hour incubation. In turn, endothelin-1 decreased permeability in endothelial cells in picomolar range, while bardoxolone methyl decreased ET-1 release and increased endothelial permeability even after short-term (3 hours) incubation. In conclusion, despite that all three Nrf2 activators exerted some beneficial effects on the endothelium, as evidenced by a decrease in ROS production, bardoxolone methyl, the most potent Nrf2 activator among the tested compounds, displayed a distinct endothelial profile of activity comprising detrimental effects on mitochondria and cellular viability and suppression of endothelial ET-1 release possibly interfering with ET-1–dependent local regulation of endothelial permeability.
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Pesic, Srdjan, Miroslav Radenkovic, and Leposava Grbovic. "Endothelial dysfunction: Mechanisms of development and therapeutic options." Medical review 59, no. 7-8 (2006): 335–41. http://dx.doi.org/10.2298/mpns0608335p.
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Introduction. Vascular endothelial cells play a key role in cardiovascular regulation by producing a number of potent vasoactive agents, including the vasodilator molecule nitric oxide (NO) and the vasoconstrictor peptide endothelin (ET). Endothelial dysfunction. Endothelial dysfunction is recognized as the initial step in the atherosclerotic process. Impairment of NO synthesis, or increased inactivation of NO by superoxide radicals, may account for the increased peripheral vascular tone, as well as contribute to the clinical consequences of different pathophysiological conditions-which include vascular hypertrophy, increased platelet and monocyte adhesion to the endothelium, atherosclerosis, myocardial infarction and stroke. To date, most interventions attempting to improve endothelial dysfunction have targeted one or more of the numerous risk factors that can cause endothelial damage: hypertension (ACE inhibitors and calcium antagonists), hypercholesterolemia (lipid-lowering agents), cigarette smoking (cessation), sedentary lifestyle (increased physical activity), menopause (estrogen replacement therapy), and diabetes mellitus (control of metabolic abnormalities). Several pharmacologic agents have been suggested to achieve vascular protection through mechanisms that go beyond their primary therapeutic actions (ACE-and HMG-CoA reductase inhibitors). Beneficial changes to the endothelium might result from promotion of vasorelaxation, inhibition of vasoconstriction, reduction in the production of free radicals, or other mechanisms that protect the endothelium from injury. Conclusion. This study deals with the results of many experimental and clinical investigations. The possibility of using different classes of drugs was also established, including ACE inhibitors, Ca-antagonists, AT and endothelin receptor antagonists, direct activator of adenyl cyclase, statins, antioxidants, L-arginine, phosphodiesterase inhibitors, beta-blockers and organic nitrates. .
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Brutsaert, Dirk L. "Cardiac Endothelial-Myocardial Signaling: Its Role in Cardiac Growth, Contractile Performance, and Rhythmicity." Physiological Reviews 83, no. 1 (January 1, 2003): 59–115. http://dx.doi.org/10.1152/physrev.00017.2002.
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Experimental work during the past 15 years has demonstrated that endothelial cells in the heart play an obligatory role in regulating and maintaining cardiac function, in particular, at the endocardium and in the myocardial capillaries where endothelial cells directly interact with adjacent cardiomyocytes. The emerging field of targeted gene manipulation has led to the contention that cardiac endothelial-cardiomyocytal interaction is a prerequisite for normal cardiac development and growth. Some of the molecular mechanisms and cellular signals governing this interaction, such as neuregulin, vascular endothelial growth factor, and angiopoietin, continue to maintain phenotype and survival of cardiomyocytes in the adult heart. Cardiac endothelial cells, like vascular endothelial cells, also express and release a variety of auto- and paracrine agents, such as nitric oxide, endothelin, prostaglandin I2, and angiotensin II, which directly influence cardiac metabolism, growth, contractile performance, and rhythmicity of the adult heart. The synthesis, secretion, and, most importantly, the activities of these endothelium-derived substances in the heart are closely linked, interrelated, and interactive. It may therefore be simplistic to try and define their properties independently from one another. Moreover, in relation specifically to the endocardial endothelium, an active transendothelial physicochemical gradient for various ions, or blood-heart barrier, has been demonstrated. Linkage of this blood-heart barrier to the various other endothelium-mediated signaling pathways or to the putative vascular endothelium-derived hyperpolarizing factors remains to be determined. At the early stages of cardiac failure, all major cardiovascular risk factors may cause cardiac endothelial activation as an adaptive response often followed by cardiac endothelial dysfunction. Because of the interdependency of all endothelial signaling pathways, activation or disturbance of any will necessarily affect the others leading to a disturbance of their normal balance, leading to further progression of cardiac failure.
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González-Villalva, Adriana, Guadalupe Morales-Ricardes, Marcela Rojas-Lemus, Patricia Bizarro-Nevares, Nelly López-Valdez, Martha Ustarroz-Cano, María Isabel García-Peláez, et al. "El endotelio sano y su disfunción en el riesgo cardiovascular." Revista de la Facultad de Medicina 66, no. 6 (November 10, 2023): 37–52. http://dx.doi.org/10.22201/fm.24484865e.2023.66.6.07.
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The endothelium is a monolayer of flatten cells named endothelial cells that form the inner layer of the heart, blood, and lymphatic vessels. Its function is not just as a barrier, but it is a regulator of vascular permeability and tone, hemostasis, inflammation, and angiogenesis. This review is about the general aspects of vascular endothelium and endothelial dysfunction that leads to increased vascular risk. Activation and dysfunction are discussed, considering the endothelialactivation as a self-limiting process, necessary to promote inflammation and hemostasis. Endothelial dysfunction is a pathological process in which the endothelium loses its ability for self-regulation and acquires a prothrombotic and proinflammation phenotype. Endothelial dysfunction is the initial step for atherosclerosis and increased cardiovascular risk, so the main biomarkers of endothelial dysfunction are reviewed. As basic knowledge about endothelium increases, preventive or therapeutic measures can be designed as treatment or prevention the risk of its dysfunction. Key words: Healthy endothelium; activation; endothelial; endothelial dysfunction; cardiovascular risk; atherosclerosis.
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Scheglovitova, O. N., N. N. Sklyankina, N. V. Boldyreva, A. A. Babayants, I. S. Frolova, and M. R. Kapkaeva. "HUMAN INTERFERON MODULATES INFECTED VASCULAR ENDOTHELIUM FUNCTION." Annals of the Russian academy of medical sciences 69, no. 3-4 (August 21, 2015): 31–35. http://dx.doi.org/10.15690/vramn.v69.i3-4.992.
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Background: To study impact of interferon (IFN) α, β and γ on the Herpes simplex virus type 1 (HSV-1) infected endothelial cells functional activity related with participation in the inflammation development. Materials and methods: In the work endothelial cells isolated from umbilical vein were used. Intact and infected cultures were treated by interferon and in the dynamics of cultivation tested mediators in the cultural medium. Results: All investigated interferons activated the production of IL-6. IFN α, β activated the production of IL-8, while IFN γ inhibited her. IFN α and γ increased synthesis of nitrogen oxides and reduced the synthesis of endothelin-1, while IFN β activated the production of endothelin-1. Conclusion: Infection of endothelial cells isolated from umbilical vein with HSV-1 does not alter the ability of interferon in modulating of proinflammatory cyto-kines, nitric oxide and endothelin-1 synthesis. It is obvious in the body modulation manifestations of innate immunity under the influence of exogenous interferon is implemented both intact and infected with HSV-1-vascular endothelium and nature modulation is determined by the type of IFN.
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Goncharov, Nikolay V., Alexander D. Nadeev, Richard O. Jenkins, and Pavel V. Avdonin. "Markers and Biomarkers of Endothelium: When Something Is Rotten in the State." Oxidative Medicine and Cellular Longevity 2017 (2017): 1–27. http://dx.doi.org/10.1155/2017/9759735.
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Endothelium is a community of endothelial cells (ECs), which line the blood and lymphatic vessels, thus forming an interface between the tissues and the blood or lympha. This strategic position of endothelium infers its indispensable functional role in controlling vasoregulation, haemostasis, and inflammation. The state of endothelium is simultaneously the cause and effect of many diseases, and this is coupled with modifications of endothelial phenotype represented by markers and with biochemical profile of blood represented by biomarkers. In this paper, we briefly review data on the functional role of endothelium, give definitions of endothelial markers and biomarkers, touch on the methodological approaches for revealing biomarkers, present an implicit role of endothelium in some toxicological mechanistic studies, and survey the role of reactive oxygen species (ROS) in modulation of endothelial status.
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Robertson, Tom P., Philip I. Aaronson, and Jeremy P. T. Ward. "Ca2+ sensitization during sustained hypoxic pulmonary vasoconstriction is endothelium dependent." American Journal of Physiology-Lung Cellular and Molecular Physiology 284, no. 6 (June 1, 2003): L1121—L1126. http://dx.doi.org/10.1152/ajplung.00422.2002.
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The main aim of this study was to determine the effects of endothelium removal on tension and intracellular Ca2+([Ca2+]i) during hypoxic pulmonary vasoconstriction (HPV) in rat isolated intrapulmonary arteries (IPA). Rat IPA and mesenteric arteries (MA) were mounted on myographs and loaded with the Ca2+-sensitive fluorophore fura PE-3. Arteries were precontracted with prostaglandin F2α, and the effects of hypoxia were examined. HPV in isolated IPA consisted of a transient constriction superimposed on a second sustained phase. Only the latter phase was abolished by endothelial denudation. However, removal of the endothelium had no effect on [Ca2+]i at any point during HPV. The endothelin-1 antagonists BQ-123 and BQ-788 did not affect HPV, although constriction induced by 100 nM endothelin-1 was abolished. In MA, hypoxia induced an initial transient rise in tension and [Ca2+]i, followed by vasodilatation and a fall in [Ca2+]i to (but not below) prehypoxic levels. These results are consistent with sustained HPV being mediated by an endothelium-derived constrictor factor that is distinct from endothelin-1 and that elicits vasoconstriction via Ca2+sensitization.
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Lefer, A. M., and X. L. Ma. "PMN adherence to cat ischemic-reperfused mesenteric vascular endothelium under flow: role of P-selectin." Journal of Applied Physiology 76, no. 1 (January 1, 1994): 33–38. http://dx.doi.org/10.1152/jappl.1994.76.1.33.
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We studied polymorphonuclear leukocyte (PMN) adherence to cat ischemic-reperfused mesenteric artery and vein endothelia under conditions of flow in vitro. Under physiological shear rates, only a few PMNs adhered to non-ischemic-reperfused arterial and venous endothelia (11 +/- 2 and 20 +/- 3 PMN/mm2, respectively). However, after 60 min of ischemia and 20 or 120 min of reperfusion, a significant increase in PMN adherence to arterial endothelium was observed. At 20 min of reperfusion, 44 +/- 4 PMN/mm2 adhered, and at 120 min postreperfusion, 63 +/- 12 PMN/mm2 adhered (P < 0.01 from control). Moreover, a greater degree of PMN adherence occurred on the venous than on the arterial endothelium. Thus, 159 +/- 10 and 198 +/- 12 PMN/mm2 adhered to mesenteric venous endothelium isolated after 20 and 120 min reperfusion, respectively (P < 0.01 vs. arteries). Furthermore, addition of PB 1.3 (20 micrograms/ml), a monoclonal antibody against P-selectin, 5 min before perfusion with PMNs significantly attenuated the increase in PMN adherence to both arterial and venous endothelia (P < 0.01). These results indicate that PMN-endothelial interaction also occurs in conduit vessels after ischemia and reperfusion, although a more profound PMN adherence occurs in veins.