Endothelial function
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American journal of cardiology. 10A, ISSN 0002-9149 Symposium Vol. 82
64S s. : il. ; 30 cm
- MeSH
- cévní endotel patofyziologie fyziologie účinky léků MeSH
- kardiovaskulární nemoci farmakoterapie MeSH
- Publikační typ
- kongresy MeSH
- Konspekt
- Patologie. Klinická medicína
- NLK Obory
- kardiologie
- angiologie
ix, 123 s., [4] s. obr. příl. : il., tab., grafy ; 20 cm
- MeSH
- arterioskleróza MeSH
- ateroembolie MeSH
- cévní endotel MeSH
- inhibitory ACE MeSH
- kininy MeSH
- Publikační typ
- kongresy MeSH
- Konspekt
- Patologie. Klinická medicína
- NLK Obory
- angiologie
Spontánne hypertenzný potkan (SHR) je najvhodnejším a najeastejšie používaným laboratórnym modelom pre výskum esenciálnej hypertenzie (EH). Patogenéza hypertenzie u SHR sa v mnohých aspektoch podobá na EH u 3udí. V 3udskej EH, a podobne u SHR, bola pozorovaná oslabená vazorelaxácia závislá od endotelu, tzv. endotelová dysfunkcia, ktorá prispieva k zvýšenej periférnej rezistencii. Endotelová dysfunkcia je pri hypertenzii charakterizovaná zmenami v produkcii a úeinku endotelových relaxaených (EDRFs) a konstriktorických (EDCFs) faktorov. Mechanizmus oslabenia relaxácie pri hypertenzii sa spája so znížením produkcie oxidu dusnatého (NO), znížením jeho biologickej dostupnosti alebo s nadprodukciou konstriktorických faktorov. Pri hypertenzii bola dokázaná zvýšená produkcia vo3ných kyslíkových radikálov, ktorá môže byś zodpovedná za zhoršenú vazodilatáciu. Zvýšená produkcia superoxidových radikálov v endoteli môže zvyšovaś inaktiváciu NO, a tým zapríeiniś zníženie jeho biologickej dostupnosti, eo môže viesś k zníženiu vazorelaxaených odpovedí cievnej steny. Na druhej strane, u SHR boli pozorované aj potlaeené, nezmenené, ale aj zvýšené relaxácie závislé od endotelu. Zdá sa, že diskrepancie v pozorovaných výsledkoch môžu spoeívaś v metodológii, v študovanom rieeisku a tiež vo veku experimentálnych zvierat.
A number of vascular diseases, including hypertension, are characterised by endothelial dysfunction caused by alterations in the production and action of the endothelium-derived relaxing (EDRFs) and/or endothelium-derived contracting (EDCFs) factors. The spontaneously hypertensive rat (SHR) is one of the most widely studied animal models for human essential hypertension. Several similarities between human primary hypertension and hypertension in the SHR have been pointed out in both the pathophysiology and the clinical course of the hypertensive disease. In human hypertension as well as in SHR, endothelium-dependent relaxation may be attenuated and this endothelial dysfunction contributes to the increased peripheral resistance. However, various results concerning endothelium-dependent relaxation, including impairment, no change and improvement have been reported in experimental hypertension. Endothelial dysfunction in hypertension has been linked to decrease in NO bioavailability, reflecting the impaired generation of NO and/or the enhanced inactivation of NO by reactive oxygen species. There is evidence that increased vascular oxidative stress is present in SHR. Thus, it has been proposed that oxidative inactivation of NO may account for the endothelial dysfunction seen in SHR. On the other hand, several studies demonstrate elevated basal NO synthesis in SHR rats which may be an adapting mechanism, preventing them from excessive blood pressure elevation. However, the role of NO in hypertension in SHR and in humans remains still controversial. We hypothesize that the vascular bed studied, the effect of age as well as methodological aspects, such as “precontraction” with different vasoconstrictors as well as antioxidants added to the solution for determination of the vasoreactivity may contribute to the discrepancies among studies. Nevertheless, the involvement of endothelial function in hypertension remains subject of debate and further research is needed to complete our knowledge on the role of NO, reactive oxygen species and other endothelial factors in the regulation of vascular and cardiac function.
- MeSH
- biologické markery MeSH
- cévní endotel fyziologie patofyziologie MeSH
- endoteliální buňky fyziologie patologie MeSH
- financování organizované MeSH
- hypertenze MeSH
- inbrední kmeny potkanů MeSH
- laboratorní zvířata MeSH
- modely nemocí na zvířatech MeSH
- oxid dusnatý krev nedostatek MeSH
- potkani Wistar MeSH
- signální transdukce MeSH
- vazodilatace MeSH
- zvířata MeSH
- Check Tag
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- přehledy MeSH
1st ed. xi, 154 s.
Frontiers in diabetes ; vol. 9
viii, 212 s. : obr., tab., bibliogr.
Endothelial dysfunction develops early and has been shown to predict the development of clinical complications of atherosclerosis. However, the relationship between early endothelial dysfunction and the progression of arterial disease in the general population is unknown. We investigated endothelial dysfunction, risk factors, and progression of carotid intima-media thickness (cIMT) in late-middle-aged individuals at low to intermediate cardiovascular risk in a prospective study between 1997 and 2005. METHODS AND RESULTS: Brachial artery flow-mediated dilatation and cIMT were measured in 213 nonsmoking British civil servants recruited from a prospective cohort (Whitehall II study). Participants (age, 45 to 66 years) were free of clinical cardiovascular disease and diabetes mellitus. Risk factors and Framingham Risk Score were determined at baseline. cIMT was repeated 6.2+/-0.4 years later. At baseline, age, blood pressure, low-density lipoprotein cholesterol, and Framingham Risk Score correlated with cIMT. However, only flow-mediated dilatation, not risk factors or Framingham Risk Score, was associated with average annual progression of cIMT. This relationship remained significant after adjustment for risk factors whether entered as separate variables or as Framingham Risk Score. Further adjustment for waist circumference, triglycerides, and employment grade had no significant effect. CONCLUSIONS: Systemic endothelial function was associated with progression of preclinical carotid arterial disease over a 6-year period and was more closely related to cIMT changes than conventional risk factors. Thus, the relationship between endothelial dysfunction and adverse outcome is likely to be due not only to destabilization of established disease in high-risk populations but also to its impact on the evolution of the atherosclerotic substrate. Flow-mediated dilatation testing provides an integrated vascular measure that may aid the prediction of structural disease evolution and represents a potential short- to intermediate-term outcome measure for evaluation of preventive treatment strategies.
- MeSH
- ateroskleróza etiologie MeSH
- cévní endotel patofyziologie MeSH
- financování organizované MeSH
- kohortové studie MeSH
- LDL-cholesterol krev MeSH
- lidé středního věku MeSH
- lidé MeSH
- prospektivní studie MeSH
- senioři MeSH
- tunica intima patologie MeSH
- tunica media patologie MeSH
- Check Tag
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři MeSH
- ženské pohlaví MeSH
Cardiovascular diseases represent the major medical and social problem. The main idea of this article was to estimate the earliest markers of vascular system injury. Endothelial function among teenagers with arterial hypertension and dyslipidemia were studied by ultrasound method, and von Willebrand factor was determined in blood. Endothelial function was changed in 46.9% of persons. Various characters of disturbances of endothelial functions were revealed.
- MeSH
- ateroskleróza * krev patofyziologie ultrasonografie MeSH
- cévní endotel * patofyziologie ultrasonografie MeSH
- dyslipidemie diagnóza MeSH
- hypertenze diagnóza MeSH
- index tělesné hmotnosti MeSH
- lidé MeSH
- měření krevního tlaku MeSH
- mladiství MeSH
- rychlost toku krve MeSH
- triglyceridy krev MeSH
- von Willebrandův faktor * analýza fyziologie MeSH
- Check Tag
- lidé MeSH
- mladiství MeSH
- mužské pohlaví MeSH
- ženské pohlaví MeSH
BACKGROUND: Endothelial progenitor cells (EPC) involved in endothelial repair and maintenance are restored following renal transplantation. There are scarce data regarding EPC in Asian kidney allograft patients. AIM: We determined the EPC numbers in Thai renal allograft patients to compare with various other parameters. PATIENTS AND METHODS: The EPC numbers which were verified as CD 133+/VEGFR-2 cells in peripheral blood of 38 renal transplant recipients were measured by flow cytometry, and by a cell culture assay using acetylated low-density lipoprotein and Ulex europaeus agglutinin-1 immunofluorescence. Renal function calculated as estimated glomerular filtration rate (eGFR) was obtained by the abbreviated Modification of Diet in Renal Disease (MDRD) formula. RESULTS: Renal allograft patients had lower EPC numbers than normal controls (P < .05). The EPC numbers showed a significant correlation with renal allograft function (P < .05). Recipients with stable eGFR at 12 months of follow-up displayed significantly greater EPC numbers at baseline compared with those subjects who experienced a decline in eGFR (P < .05). Recipients using angiotensin receptor blockers had greater EPC numbers at baseline and better 12-month renal allograft function (P < .05). CONCLUSION: EPC numbers may influence the fate of renal allograft function. Enhancing EPC numbers may be a new strategy to improve long term renal allograft function.
- MeSH
- CD antigeny analýza MeSH
- dietoterapie MeSH
- endoteliální buňky cytologie MeSH
- glykoproteiny analýza MeSH
- hodnoty glomerulární filtrace MeSH
- homologní transplantace MeSH
- imunofenotypizace MeSH
- kmenové buňky cytologie MeSH
- lidé MeSH
- následné studie MeSH
- peptidy analýza MeSH
- počet buněk MeSH
- průtoková cytometrie MeSH
- receptor 2 pro vaskulární endoteliální růstový faktor analýza MeSH
- referenční hodnoty MeSH
- transplantace ledvin fyziologie MeSH
- vyšetření funkce ledvin MeSH
- Check Tag
- lidé MeSH
Endothelial cell (EC) glycocalyx (GLX) comprise a multicomponent layer of proteoglycans and glycoproteins. Alteration of its integrity contributes to chronic vascular inflammation and leads to the development of cardiovascular diseases. Myeloperoxidase (MPO), a highly abundant enzyme released by polymorphonuclear neutrophils, binds to the GLX and deleteriously affects vascular EC functions. The focus of this study was to elucidate the mechanisms of MPO-mediated alteration of GLX molecules, and to unravel subsequent changes in endothelial integrity and function. MPO binding to GLX of human ECs and subsequent internalization was mediated by cell surface heparan sulfate chains. Moreover, interaction of MPO, which is carrying a cationic charge, with anionic glycosaminoglycans (GAGs) resulted in reduction of their relative charge. By means of micro-viscometry and atomic force microscopy, we disclosed that MPO can crosslink GAG chains. MPO-dependent modulation of GLX structure was further supported by alteration of wheat germ agglutinin staining. Increased expression of ICAM-1 documented endothelial cell activation by both catalytically active and also inactive MPO. Furthermore, MPO increased vascular permeability connected with reorganization of intracellular junctions, however, this was dependent on MPO's catalytic activity. Novel proteins interacting with MPO during transcytosis were identified by proteomic analysis. Altogether, these findings provide evidence that MPO through interaction with GAGs modulates overall charge of the GLX, causing modification of its structure and thus affecting EC function. Importantly, our results also suggest a number of proteins interacting with MPO that possess a variety of cellular localizations and functions.
- MeSH
- cévní endotel MeSH
- endoteliální buňky MeSH
- lidé MeSH
- neutrofily MeSH
- peroxidasa * MeSH
- proteomika * MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
