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Hypertension and nephrology

FEBRUARY 20, 2020

Hypertension and nephrology

DECEMBER 20, 2016

[Deeper analysis of nebivolol effects]

KÉKES Ede

[Author presents the formation of nitric oxide as a largest vasodilator of human endothelium as well as the endothelial dysfunction a result of formation at adrenergic stimulus. He demonstrates in detail the benefits of selective β-1 blocker and β-3 adrenergic agonist nebivolol in the vascular system. This drug has also receptor independent effects. Complex effects of nebivolol causes vasodilation, inhibits oxidative stress and it is capable to neutralize the effects of free oxygen radicals and as a result the endothelial function will be better. Its clinical effects and the less wellknown beneficial properties are listed. The use of drug is discussed especially in hypertensives with smoking, COPD or PAD. The β-3 agonist effect provides positive reactions not only in the adipocytes and the myocardial tissue. but in the skeletal muscle as well: Increase in energy expenditure - as a compensatory mechanism - is increased in obesity and the glucose uptake + storage on skeletal muscle cells are increased in hyperglycemia. The insulin sensitivity will be better, leptin level is decreased, adiponectin level is increased by nebivolol. It is assumed this drug has antidiabetic and anti-obesity effects.]

Hypertension and nephrology

FEBRUARY 20, 2014

[Fenestration of endothelium of juxtaglomerular arteriole]

ROSIVALL László

[For the first time, we demonstrated the fenestration in the endothelium of the distal portion of renal afferent arteriole (AA), which is unusual among high pressure vessels. The fenestrae are co-localized with renin producing granular epithelioid cells; this arrangement makes it likely that the relatively large renin molecules may use this path to enter into the plasma. We also demonstrated that the length and area of this fenestrated segment 1) correlates with the activity of the renin-angiotensin system (RAS), 2) may change by age, in response to some stimuli such as thirst and in some diseases, 3) allows filtration of fluid prior to the glomerular filtration, which can be as high as about 30% of GFR. This morphology and the high filtration volume in AA is one of the most striking observations of renal microcirculation, and question several basic renal physiological issues.]

Hypertension and nephrology

OCTOBER 20, 2013

[The role of juxtaglomerular apparatus in regulation of renal hemodinamics]

ROSIVALL László

[The tubuloglomerular feedback mechanism (TGF) is one of the basic processes in the regulation of renal microcirculation. During the activation of TGF the macula densa senses the tubular fluid and ions loads and initiates a rather complex mechanism in juxtaglomerular apparatus resulting in a change of GFR and tubular load. During the activation of TGF there is humoral signaling in the interstitial extraglomerular area. The concentration of the mediator depends on the extraglomerular interstitial fluid movement through the fenestrated endothelium, which is determined by the actual pressures. A new and fast GFR regulation mechanism is described as a consequence.]

Hypertension and nephrology

DECEMBER 30, 2012

[The apparatus which controls our kidney too. Part 2 - Structure and function of the juxtaglomerular apparatus]

ROSIVALL László

[The juxtaglomerular apparatus is comprised of the macula densa (a specialregion of the distal tubule), the renin producing granular or epithelioid-cells of the afferent arteriole, the extraglomerular mesengial cells, and the efferent arteriole’s section bordering this region. Somewhat more general definitions also exist. Recently, distinctive morphological and functional associations have been identified between the components of the JGA and some common mediators (e.g. adenosine, angiotensin, NO, prostaglandins, etc.). Current data suggest that each cell of the macula densa also contain few cilia that may have a role in sensing fluid flow. The distal section of the afferent arteriole (possessing the same structure as the glomerular capillaries) is covered by fenestrated endothelium. Trace dose of ferritin particles can pass through the afferent arteriole’s fenestrae into the interstitium of the JGA due to the considerable hydrostatic pressure gradient. The parietal lamina of Bowman’s capsule, which covers the renin granulated cells of the afferent arteriole behaves much like the visceral lamina in that the epithelial cells of the parietal lamina exhibit foot processes and filtration slits. The urinary space is regularly bulging into the extraglomerular mesangium. Therefore, the notion has been refuted that the JGA, which contains neither blood nor lymph capillaries, is a closed system engaging in only slow fluid exchange. Furthermore it is affirmed that the afferent arteriole consists of two morphologically and functionally disparate segments, the ratio of which is considerably modified by the activity of the renin-angiotensin system.]

Lege Artis Medicinae

SEPTEMBER 10, 2001

[Endothel dysfunction and hypertension]

KELEMEN Judit, BLASKÓ György

[In the past two decade numerous data has been collected about the role of endothelium in the development of several cardiovascular disorders i.e. hypertension, congestive heart failure and atherosclerosis. Endothelial cells had been thought to be passive barriers only, but it turned out that through paracrine and autocrine hormone secretion they take part in modulating and regulating the vasodilator and vasoconstrictor effects being directed to vascular smooth muscle cells. The intact endothelium prevents the adhesion of platelets and monocytes, the platelet aggregation, as well as the migration and proliferation of vascular smooth muscle cells. It has been shown that both in experimental and human hypertension the endothelial function i.e. the so-called endothel-dependent vasodilatation is damaged, being the main feature of endothelial dysfunction. In spite of extensive research it is not clear whether endothelial dysfunction is a cause or a consequence of hypertension, with exact pathomechanism being also unclear. Methods, by which this important parameter could be precisely measured are under development. Researchers also examine whether recently used antihypertensive agents could improve or eliminate endothelial dysfunction and whether this effect may offer benefit to patients in terms of morbidity and mortality. This article attempts to summarize the most up-to-date information about the endothelial dysfunction research.]

Hungarian Immunology

JANUARY 22, 2008

[The role of endothelium, cell migration, chemokines and angiogenesis in inflammatory rheumatic diseases]

BESENYEI Tímea, PÁKOZDI Angéla, VÉGVÁRI Anikó, SZABÓ Zoltán, SZEKANECZ Zoltán

[Endothelial cells, leukocyte-endothelial interactions and angiogenesis are highly involved in the pathogenesis of inflammation and thus in that of inflammatory rheumatic diseases. As this research area is very progressive, one needs to review novel molecular mechanisms and new therapeutic approaches in this respect. Authors review the most important functions of endothelial cells, the process of leukocyte extravasation, tissue infiltration and their cellular and molecular basis. Endothelial cells themselves produce a number of inflammatory mediators including interleukin-1 (IL-1), IL-6, IL-8, chemokines and others. Among cell adhesion molecules, β1 and β3 integrins, as well as E-, L- and P-selectins and their respective ligands have been implicated in leukocyte-endothelial adhesion. In recent years, numerous inflammatory mediators, cytokines, chemokines and proteases have been implicated in angiogenesis and angiostasis. Hypoxia, the vascular endothelial growth factor (VEGF)-angiopoietin system and mechanisms driven by β3 integrins are of major importance during angiogenesis. Significant amount of data have become available of the regulation of cell adhesion, migration and neovascularisation. Adhesion, chemokine and angiogenesis research has important clinical, practical aspects for antirheumatic and anti-cancer therapy. VEGF antagonists, anti-integrin antibodies, chemokine and chemokine receptor inhibitors, as well as thalidomide are currently in the first line of development.]

Hungarian Immunology

JANUARY 30, 2006

[Regional cues and phenotypic responses during the ontogeny and postnatal development of splenic vasculatur]

BALOGH Péter

[Among structured peripheral lymphoid tissues in man and rodents, the spleen demonstrates the most extensive flexibility in functional activities, which is coupled with considerable tissue architecture adjustments during ontogeny and immune reactions. The sequential conversion of a primary lymphohemopoietic tissue into a major peripheral lymphoid organ (while participating in the post-myeloid period of primary B-lymphopoiesis and retaining the potential for myelopoiesis) is accompanied with the ordered segregation involving various non-hemopoietic components of architecture, including the endothelia of blood vessels. In this report we will survey the functional and structural aspects of heterogeneous endothelial cells lining the various splenic vascular beds, comprising the complex circulatory network of the spleen. These features will be correlated with the characteristics of those regulatory mechanisms that have recently been demonstrated to be responsible for the establishment and maintenance of the endothelial divergence during splenic vascular development, including crucial transcription factors, morphogenic regulatory ligands and receptors of the tumor necrosis factor/lymphotoxin (TNF/LT) family and others. The influence of these regulatory elements in mice appears to be highly restricted in terms of regional involvement of the vasculature, with cellular alterations of the marginal sinus representing the most frequently affected region. This complexity highlights the importance of this tissue region in both the formation of splenic vasculature and a possible source for white pulp stromal elements as well as its function as a major gateway for lymphocyte traffic.]

Lege Artis Medicinae

JULY 20, 2004

[ENDOTHELIUM PROTECTION IN HYPERTENSIVE PATIENTS]

KÉKES Ede

[The author presents a review about the fundamental principles of normal endothelial function and the main causes for the development of endothelial dysfunction. First of all, endothelial dysfunction results in structural alterations in the wall of the vessel - the „vascular remodelling” in hypertension - and that is the base of hypertensive microangiopathy and target organ damage. In patients with high blood pressure the reactivity of vessels is impaired by the endothelial dysfunction. The members of the main drug groups can influence the vasoactive factors produced in endothelium differently. This different effects of drugs create different clinical benefits. Especially, the ACE inhibitors, the calcium antagonists (mostly the new generation of dihydropyridines) have endothelial protective effects, but some β-blockers, α-1 adrenergic blockers and - in a totally different way of action - the statins are capable of influencing the endothelial dysfunction.]

Lege Artis Medicinae

JANUARY 27, 2009

[Importance of statin therapy in stroke prevention]

KÁPOSZTA Zoltán, RÁCZ Klára

[Stroke is the third leading cause of death and a leading cause of major adult disability in developed countries. The annual incidence of hospitalized stroke varies between 400-500 per 100 000 inhabitants every year in Hungary. In the past decade, cholesterol lowering with 3- hydroxy-3-methylglutaryl-coenzyme A (HMGCoA) reductase inhibitors (statins) has proved to reduce risk of stroke in patients with and without coronary disease (CAD). In patients with CAD, statin therapy reduces the risk of first stroke by 25% to 35% versus placebo and, moreover, intensive statin therapy to LDL-C targets below 2.6 mmol/L (100 mg/dL) appears to reduce the risk further. More recently it has also been shown that intensive statin therapy can reduce risk of recurrent stroke in nondiabetic as well as diabetic patients with recent stroke or transient ischaemic attack but no CAD. The overall reduction of stroke and TIA was 23%. Evidence from retrospective studies suggests that in addition to risk reduction statin pretreatment may improve stroke outcome. It may due to their pleiotropic effects that include improvement of endothelium function, anti-inflammatory, antithrombotic, and immunomodulatory effects. As statins have both an excellent safety profile and simple administration, physicians should consider using statins, at dosages shown to have efficacy in clinical trials, in all patients whose cardiovascular risk profile puts them at high risk of stroke.]