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81. Systems analysis in hypertension: complementary role of physiologists and geneticists

Creator:
Josef Zicha, Ivana Vaněčková, and Jaroslav Kuneš
Format:
print, bez média, and svazek
Type:
article, úvodníky, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, hypertenze, fyziologie, genetika, hypertension, physiology, genetics, 14, and 612
Language:
English
Description:
J. Zicha, I. Vaněčková, J. Kuneš. and Obsahuje bibliografii
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

83. The dilemma of dual renin-angiotensin system blockade in chronic kidney disease: why beneficial in animal experiments but not in the clinic?

Creator:
Věra Čertíková-Chábová and Luděk Červenka
Format:
print, bez média, and svazek
Type:
article, články, journal articles, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, inhibitory angiotenzin konvertujícího enzymu, hypertenze, angiotensin converting enzyme inhibitors, hypertension, renin-angiotensin system, angiotensin II type 1 receptor antagonists, chronic kidney diseases, 14, and 612
Language:
English
Description:
Drugs interfering with the renin-angiotensin-aldosterone system (RAAS) improved the prognosis in patients with hypertension, heart failure, diabetes and chronic kidney disease. However, combining different drugs brought no further benefit while increasing the risk of hyperkalemia, hypotension and acute renal failure. This was so with combining angiotensin converting enzyme inhibitors (ACEi) and angiotensin II receptors type 1 antagonists (ARB). Dissimilarly, in animal disease models this dual therapy proved clearly superior to single drug treatment and became the optimal standard regime for comparison with other treatments. This review analyzes the causes of the discrepancy of effects of the dual therapy between animal experiments versus clinical studies, and is focused on the outcomes in chronic kidney disease. Discussed is the role of species differences in RAAS, of the variability of the disease features in humans versus relative stability in animals, of the genetic uniformity in the animals but not in humans, and of the biased publication habits of experimental versus clinical studies. We attempt to understand the causes and reconcile the discordant findings and suggest to what extent dual RAAS inhibition should be continued in animal experiments and why its application in the clinics should be limited to strictly selected groups of patients., V. Čertíková Chábová, L. Červenka., and Obsahuje bibliografii
Rights:
http://creativecommons.org/publicdomain/mark/1.0/ and policy:public

84. The effect of hypertension on adult hippocampal neurogenesis in young adult spontaneously hypertensive rats and Dahl rats

Creator:
Pistikova, A., Brozka, H., Bencze, M., Radostova, D., Vales, K., and Stuchlik, A.
Type:
article, model:article, and TEXT
Subject:
adult neurogenesis, captopril, hypertension, dahl rats, SHR, and young animals
Language:
English
Description:
The dentate gyrus of the hippocampus is one of the few places in the brain where neurogenesis occurs in adulthood. Nowadays, an increasing number of children and young adults are affected by hypertension, one of the factors in the development of cerebrovascular diseases and age-related cognitive deficits. Since these cognitive deficits are often hippocampus-dependent, it is possible that hypertension exerts this effect via decreasing adult neurogenesis which has been shown to be essential for a range of cognitive tasks. We used spontaneously hypertensive rats, which develop hypertension in the first weeks of life. Half of them were treated with the antihypertensive drug captopril. We found that the drug-induced lowering of blood pressure in this period did not affect the rate of adult neurogenesis. In a second experiment, we used another animal model of hypertension – salt-sensitive and salt-resistant strains of Dahl rats. A high-salt diet induces hypertension in the salt-sensitive strain, but not in the salt-resistant strain. The high-salt diet led to salt-induced hypertension, but did not affect the level of adult neurogenesis in the dentate gyrus of the hippocampus. We conclude that hypertension does not significantly affect the rate of hippocampal neurogenesis in young adult rats.
Rights:
http://creativecommons.org/publicdomain/mark/1.0/ and policy:public

85. The effect of obesity, hypertension, diabetes mellitus, alcohol, and sleep apnea on the risk of atrial fibrillation

Creator:
Čarná, Zuzana and Osmančík, Pavel
Format:
počítač and online zdroj
Type:
model:article and TEXT
Subject:
atrial fibrillation, obesity, hypertension, and risk factor modification
Language:
English
Description:
Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia associated with a two-fold increase in mortality caused by a higher risk of stroke and heart failure. Currently, AF is present in ~ 2 % of the general population, and its incidence and prevalence are increasing. Obesity, hypertension, diabetes mellitus, obstructive sleep apnea, and alcohol consumption increase the risk of AF. Each unit of increase in BMI increases the risk of AF by 3 %, and intensive weight loss is also associated with reduced AF recurrence. Hypertension increases the risk of AF by 50 % in men and by 40 % in women, and explains ≈ 20 % of new AF cases. Patients with obstructive sleep apnea are at four times higher risk of developing AF than subjects without sleep apnea. Higher concentrations of pro-inflammatory cytokines, higher amounts of epicardial adipose tissue, and a higher degree of ventricular diffuse myocardial fibrosis are present in AF patients and patients with the aforementioned metabolic disorders. Several prospective cohort studies and randomized trials have been initiated to show whether weight loss and treatment of other risk factors will be associated with a reduction in AF recurrences.
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

86. The interaction of genetic and environmental factors in the etiology of hypertension

Creator:
Jaroslav Kuneš and Josef Zicha
Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, fyziologie, syndrom inzulinové rezistence, hypertenze, geny, životní prostředí, ekologická genetika, physiology, insulin resistance syndrome, hypertension, genes, environment, ecological genetics, 14, and 612
Language:
English
Description:
Essential hypertension is a major risk factor for several cardiovascular diseases. It is a complex trait resulting from the interactions of multiple genetic and environmental factors. Moreover, not only genetic but also epigenetic inheritance plays a significant role. One can speculate that hypertension develops as a consequence of “errors” in well-coordinated regulatory systems of blood pressure. Errors in the cascade of molecular, biochemical and genetic processes, which regulate blood pressure, have finally enough potential to result in hypertension. Numerous environmental factors surrounding the organism during its development should influence the expression of genetic information. However, despite the considerable research effort, it is still difficult to identify all genes and/or other genetic determinants leading to essential hypertension and other cardiovascular diseases. This is mainly because these diseases usually become a medical problem in adulthood, although their roots might be traced back to earlier stages of ontogeny. The link between distinct developmental periods (e.g. birth and adulthood) should involve changes in gene expression involving epigenetic phenomena. The purpose of the present paper is to bring a piece of light on gene-environmental interactions potentially implicated in the pathogenesis of hypertension., J. Kuneš, J. Zicha., and Obsahuje seznam literatury
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

87. The onset of apoptosis of neurons induced by ischemia-reperfusion injury is delayed by transient period of hypertension in rats

Creator:
Martin Smrčka, Marcel Horký, Filip Otevřel, Šárka Kuchtíčková, Vladimír Kotala, and Jan Mužík
Format:
print, bez média, and svazek
Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, hypertenze, apoptóza, hypertension, apoptosis, neuroprotection, MADD, PARP-1, Caspase-3, 14, and 612
Language:
English
Description:
a1_We investigated the potential neuroprotective effect of transient hypertension on neuronal cell death induced by ischemia-reperfusion. Recovery of neurons, terminally differentiated cells, is almost entirely dependent upon active transcription and repair of DNA damage. We focused on the histochemical detection of distribution of NOR (argyrophylic nucleolar proteins) reflecting nucleolar integrity, immunohistochemical detection of PARP-1 (poly(ADP-ribose) polymerase-1), MADD (mitogen-activated death domain), a protein accumulated in nucleoli upon stimulation by ischemia, the active form of caspase-3, a universal proteolytic enzyme of apoptosis. The terminal deoxynucleotidyl-transferase (TdT)-mediated dUTP-biotin nick-end-labeling method (TUNEL) proved the presence of in situ DNA fragmentation. We used the model of transient focal cerebral ischemia in rats with occlusion of middle cerebral artery. In experimental group of rats, the transient hypertension was induced by constriction of the abdominal aorta. The period of ischemia lasted 15, 30, 60 and 120 min followed by 48 h of reperfusion. We examined the frontal lobe of the ipsilateral hemisphere for apoptosis of neurons and compared it with the intact brain tissue. In normotensive rats with transient focal cerebral ischemia, we found disintegrated nucleoli of cortical as well as subcortical neurons at all investigated periods of ischemia, whereas the neurons of intact animals showed compact nucleoli with a few satellites. Nuclear positivity for MADD and PARP-1 was apparent in the neocortex after 15 min and peaked after 30 min of ischemia. On the other hand, the subcortical neurons showed nuclear positivity after 60 and 120 min. The immunohistochemical reaction for active caspase 3 was apparent after 30 min onwards predominantly in the cortex. The TUNEL staining was distinct after 60 and 120 min., a2_In hypertensive rats, we found nucleolar disintegration, positivity for MADD, PARP-1 and caspase 3 after 30 min cortically and subcortically, followed by TUNEL positive staining of cortical neurons after 60 and 120 min. In summary, we detected delayed activation of neuronal apoptosis in transiently hypertensive rats with focal cerebral ischemia compared to normotensive animals. The apoptotic phenotype was confirmed by a panel of complementary methods showing rapid proteolysis-nucleolar segregation, MADD, PARP-1 and caspase-3 positivity as well as ultimate DNA fragmentation proved by the TUNEL assay., M. Smrčka, M. Horký, F. Otevřel, Š. Kuchtíčková, V. Kotala, J. Mužík., and Obsahuje bibliografii
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

88. The role of nitric oxide in the maintenance of vasoactive balance

Creator:
Oľga Pecháňová and Fedor Šimko
Format:
print, bez média, and svazek
Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, oxid dusnatý, endoteliální dysfunkce, hypertenze, nitric oxide, endothelial dysfunction, hypertension, angiotensin II, endothelins, reactive oxygen species, 14, and 612
Language:
English
Description:
Endothelial dysfunction may be considered as the interstage between risk factors and cardiovascular pathology. An imbalance between the production of vasorelaxing and vasoconstricting factors plays a decisive role in the development of hypertension, atherosclerosis and target organ damage. Except vasorelaxing and antiproliferative properties per se, nitric oxide participates in antagonizing vasoconstrictive and growth promoting effects of angiotensin II, endothelins and reactive oxygen species. Angiotensin II is a potent activator of NAD(P)H oxidase contributing to the production of reactive oxygen species. Numerous signaling pathways activated in response to angiotensin II and endothelin-1 are mediated through the increased level of oxidative stress, which seems to be in casual relation to a number of cardiovascular disturbances including hypertension. With respect to the oxidative stress, the NO molecule seems to be of ambivalent nature. On the one hand, NO is able to reduce generation of reactive oxygen species by inhibiting association of NAD(P)H oxidase subunits. On the other hand, when excessively produced, NO reacts with superoxides resulting in the formation of peroxynitrite, which is a free radical deteriorating endothelial function. The balance between vasorelaxing and vasoconstricting substances appears to be the principal issue for the physiological functioning of the vascular bed., O. Pecháňová, F. Šimko., and Obsahuje bibliografii
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

89. The role of Nrf2 and PPARγ in the improvement of oxidative stress in hypertension and cardiovascular diseases

Creator:
Dovinova, Ima, Kvandova, Miroslava, Balis, Peter, Gresova, Linda, Majzunova, Miroslava, Horakova, Lubica, Chan, Julie Y. H., and Barancik, Miroslav
Format:
počítač and online zdroj
Type:
model:article and TEXT
Subject:
Nrf2, PPARγ, oxidative stress, redox regulation, hypertension, and cardiovascular diseases
Language:
English
Description:
Reactive oxygen species are an important element of redox regulation in cells and tissues. During physiological processes, molecules undergo chemical changes caused by reduction and oxidation reactions. Free radicals are involved in interactions with other molecules, leading to oxidative stress. Oxidative stress works two ways depending on the levels of oxidizing agents and products. Excessive action of oxidizing agents damages biomolecules, while a moderate physiological level of oxidative stress (oxidative eustress) is necessary to control life processes through redox signaling required for normal cellular operation. High levels of reactive oxygen species (ROS) mediate pathological changes. Oxidative stress helps to regulate cellular phenotypes in physiological and pathological conditions. Nrf2 (nuclear factor erythroid 2-related factor 2, NFE2L2) transcription factor functions as a target nuclear receptor against oxidative stress and is a key factor in redox regulation in hypertension and cardiovascular disease. Nrf2 mediates transcriptional regulation of a variety of target genes. The Keap1-Nrf2-ARE system regulates many detoxification and antioxidant enzymes in cells after the exposure to reactive oxygen species and electrophiles. Activation of Nrf2/ARE signaling is differentially regulated during acute and chronic stress. and Keap1 normally maintains Nrf2 in the cytosol and stimulates its degradation through ubiquitination. During acute oxidative stress, oxidized molecules modify the interaction of Nrf2 and Keap1, when Nrf2 is released from the cytoplasm into the nucleus where it binds to the antioxidant response element (ARE). This triggers the expression of antioxidant and detoxification genes. The consequence of long-term chronic oxidative stress is activation of glycogen synthase kinase 3β (GSK-3β) inhibiting Nrf2 activity and function. PPARγ (peroxisome proliferator-activated receptor gamma) is a nuclear receptor playing an important role in the management of cardiovascular diseases, hypertension and metabolic syndrome. PPARγ targeting of genes with peroxisome proliferator response element (PPRE) has led to the identification of several genes involved in lipid metabolism or oxidative stress. PPARγ stimulation is triggered by endogenous and exogenous ligands – agonists and it is involved in the activation of several cellular signaling pathways involved in oxidative stress response, such as the PI3K/Akt/NOS pathway. Nrf2 and PPARγ are linked together with their several activators and Nrf2/ARE and PPARγ/PPRE pathways can control several types of diseases.
Rights:
http://creativecommons.org/publicdomain/mark/1.0/ and policy:public

90. The role of renin-angiotensin system in prothrombotic state in essential hypertension

Creator:
Anna Remková and Milan Remko
Format:
print
Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, endotel, hypertenze, endothelium, hypertension, platelet, coagulation, fibrionolysis, 14, and 612
Language:
English
Description:
Rheological, haemostatic, endothelial and platelet abnormalities appear to play a role in the thrombotic complications of hypertension. This prothrombotic/hypercoagulable state in hypertension may contribute to the increased risk and severity of target organ damage. It can be induced by the activated reninangiotensin system (RAS), with abnormalities in endothelial and platelet function, coagulation and fibrinolysis. Treatment of uncomplicated essential hypertension by RAS targeting antihypertensive therapy could result in a reversal of prothrombotic abnormalities, contributing to a reduction of thrombosis-related complications. Since angiotensin converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) have two distinct mechanisms of RAS interruption, it is hypothesized that each therapy might have different impact on the prothrombotic state in hypertensive patients. Some studies demonstrate a beneficial effect of both ACE inhibitors and ARBs on prothrombotic state, in addition to their efficacy to normalize elevated blood pressure. The potentially antithrombotic effect of the RAS inhibiting agents may in turn support the preservation of cardiovascular function. Available data may offer an additional explanation for the efficacy of the RAS targeting agents in the prevention of cardiovascular events in patients with atherosclerotic vascular disease., A. Remková, M. Remko., and Obsahuje bibliografii a bibliografické odkazy
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public