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32. Inactivation of Gi proteins by pertussis toxin diminishes the effectiveness of adrenergic stimuli in conduit arteries from spontaneously hypertensive rats

Creator:
Zemančíková, A., Török, J., Josef Zicha, and Jaroslav Kuneš
Format:
print, bez média, and svazek
Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, fyziologie, hypertenze, tepny, physiology, hypertension, arteries, pertussis toxin, adrenergic contractions, conduit arteries, angiotensin II, Gi proteins, 14, and 612
Language:
English
Description:
Treatment with pertussis toxin (PTX) which eliminates the activity of Gi proteins effectively reduces blood pressure (BP) and vascular resistance in spontaneously hypertensive rats (SHR). In this study we have compared the functional characteristics of isolated arteries from SHR with and without PTX-treatment (10 μg/kg i.v., 48 h before the experiment). Rings of thoracic aorta, superior mesenteric artery and main pulmonary artery were studied under isometric conditions to measure the reactivity of these vessels to receptor agonists and to transmural electrical stimuli. We have found that the treatment of SHR with PTX had no effect on endothelium-dependent relaxation of thoracic aorta induced by acetylcholine. In PTX-treated SHR, the maximum contraction of mesenteric artery to exogenous noradrenaline was reduced and the dose-response curve to cumulative concentration of noradrenaline was shifted to the right. Similarly, a reduction in the magnitude of neurogenic contractions elicited by electrical stimulation of perivascular nerves was observed in the mesenteric artery from PTX-treated SHR. PTX treatment of SHR also abolished the potentiating effect of angiotensin II on neurogenic contractions of the main pulmonary artery. These results indicate that PTX treatment markedly diminishes the effectiveness of adrenergic stimuli in vasculature of SHR. This could importantly affect BP regulation in genetic hypertension., A. Zemančíková, J. Török, J. Zicha, J. Kuneš., and Obsahuje bibliografii a bibliografické odkazy
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

33. Indapamide-induced prevention of myocardial fibrosis in spontaneous hypertension rats is not nitric oxide-related

Creator:
Pavol Janega, Kojšová, S., Lýdia Jendeková, Pavel Babál, and Oľga Pecháňová
Format:
print, bez média, and svazek
Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, fyziologie, hypertenze, oxid dusnatý, physiology, hypertension, nitric oxide, fibróza myokardu, indapamid, myocardial fibrosis, indapamide, 14, and 612
Language:
English
Description:
We studied the effect of thiazide-like diuretic – indapamide on fibrosis development in the left ventricle of young spontaneously hypertensive rats (SHR) and assessed the involvement of nitric oxide in this process. Six-week-old male SHR were treated with indapamide (1 mg/kg/day) for six weeks. Age-matched SHR were used as hypertensive and Wistar-Kyoto rats (WKY) as normotensive control. Systolic blood pressure was measured by tail-cuff plethysmography. Nitric oxide synthase (NOS) activity, protein expressions of endothelial (eNOS) and inducible NOS (iNOS), myocardial fibrosis and collagen type I and III were determined in the left ventricle. Indapamide treatment partially prevented SBP increase in SHR (SHR+Indapamide: 157±4, SHR: 171±3, WKY: 119±3 mmHg). Indapamide prevented myocardial fibrosis development in SHR, but without affecting collagen type I to type III ratio. Indapamide did not affect NOS activity as well as eNOS and iNOS protein expressions in the left ventricles evaluated by both Western blot and immunohistochemically. In conclusion, our results indicate that indapamide-induced prevention of myocardial fibrosis is not mediated by nitric oxide-related mechanism., P. Janega, S. Kojšová, L. Jendeková, P. Babál, O. Pecháňová., and Obsahuje bibliografii a bibliografické odkazy
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

34. Intrapulmonary activation of the angiotensin-converting enzyme type 2/angiotensin 1-7/G-protein-coupled Mas receptor axis attenuates pulmonary hypertension in Ren-2 transgenic rats exposed to chronic hypoxia

Creator:
Václav Hampl, Jan Herget, Jana Bíbová, Alena Baňasová, Zuzana Husková, Zdeňka Vaňourková, Jíchová, Š., Kujal, P., Zdenka Vernerová, Sadowski, J., and Luděk Červenka
Format:
print, bez média, and svazek
Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, hypertenze, hypertension, hypoxic pulmonary hypertension, renin-angiotensin system, 14, and 612
Language:
English
Description:
The present study was performed to evaluate the role of intrapulmonary activity of the two axes of the renin-angiotensin system (RAS): vasoconstrictor angiotensin-converting enzyme (ACE)/angiotensin II (ANG II)/ANG II type 1 receptor (AT 1 ) axis, and vasodilator ACE type 2 (ACE2)/angiotensin 1-7 (ANG 1-7)/ Mas receptor axis, in the development of hypoxic pulmonary hypertension in Ren-2 transgenic rats (TGR). Transgene-negative Hannover Sprague-Dawley (HanSD) ra ts served as controls. Both TGR and HanSD rats responded to two weeks' exposure to hypoxia with a significant increase in mean pulmonary arterial pressure (MPAP), however, the increase was much less pronounced in the former. The attenuation of hypoxic pulmonary hypertension in TGR as compared to HanSD rats was associated with inhibition of ACE gene expression and activity, inhibition of AT 1 receptor gene expression and suppression of ANG II levels in lung tissue. Simultaneously, there was an increase in lung ACE2 gene expression and activity and, in particular, ANG 1-7 concentrations and Mas receptor gene expression. We propose that a combination of su ppression of ACE/ANG II/AT 1 receptor axis and activation of ACE2/ANG 1-7/Mas receptor axis of the RAS in the lung tissue is the main mechanism explaining attenuation of hypoxic pulmonary hypertension in TGR as compared with HanSD rats., V. Hampl, J. Herget, J. Bíbová, A. Baňasová, Z. Husková, Z. Vaňourková, Š. Jíchová, P. Kujal, Z. Vernerová, J. Sadowski, L. Červenka., and Obsahuje bibliografii
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

35. Involvement of BKCa and KV potassium channels in cAMP-induced vasodilatation: their insufficient function in genetic hypertension

Creator:
Mária Pintérová, Behuliak, M., Jaroslav Kuneš, and Josef Zicha
Format:
print, bez média, and svazek
Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, hypertenze, hypertension, isoprenaline, cyclic AMP, potassium channels, genetic hypertension, calcium channels, 14, and 612
Language:
English
Description:
Spontaneously hypertensive rats (SHR) are characterized by enhanced sympathetic vasoconstriction, whereas their vasodilator mechanisms are relatively attenuated compared to their high BP. The objective of our in vivo study was to evaluate whether the impaired function of BKCa and/or KV channels is responsible for abnormal cAMP-induced vasodilatation in genetic hypertension. Using conscious SHR and normotensive WKY rats we have shown that under the basal conditions cAMP overproduction elicited by the infusion of β-adrenoceptor agonist (isoprenaline) caused a more pronounced decrease of baseline blood pressure (BP) in SHR compared to WKY rats. Isoprenaline infusion prevented BP rises induced by acute NO synthase blockade in both strains and it also completely abolished the fully developed BP response to NO synthase blockade. These cAMP-induced vasodilator effects were diminished by the inhibition of either BKCa or KV channels in SHR but simultaneous blockade of both K+ channel types was necessary in WKY rats. Under basal conditions, the vasodilator action of both K+ channels was enhanced in SHR compared to WKY rats. However, the overall contribution of K+ channels to cAMP-induced vasodilator mechanisms is insufficient in genetic hypertension since a concurrent activation of both K+ channels by cAMP overproduction is necessary for the prevention of BP rise elicited by acute NO/cGMP deficiency in SHR. This might be caused by less effective activation of these K+ channels by cAMP in SHR. In conclusion, K+ channels seem to have higher activity in SHR, but their vasodilator action cannot match sufficiently the augmented vasoconstriction in this hypertensive strain., M. Pintérová, M. Behuliak, J. Kuneš, J. Zicha., and Obsahuje bibliografii
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

36. Jak prospívá střídmé pití vína lidskému zdraví?

Creator:
Šamánek, Milan and Urbanová, Zuzana
Format:
braille, text, and regular print
Type:
model:article, article, Text, and TEXT
Subject:
pití alkoholu, víno--dějiny--využití, dějiny lékařství, kardiovaskulární nemoci--prevence a kontrola, klinické zkoušky jako téma, ženské pohlaví, mužské pohlaví, lidé středního věku, staří, staří nad 80 let, lidé, diabetes mellitus--prevence a kontrola, hypertenze--prevence a kontrola, cévní mozková příhoda--prevence a kontrola, infarkt myokardu--prevence a kontrola, stáří, hypertenze, diabetes, cévní mozková příhoda, and infarkt mykoardu
Language:
Czech and English
Description:
Víno pijeme nejméně 10 000 let nebo déle, v našem regionu již od doby keltské a germánské. Pokus používat víno k léčbě začíná v dávnověku, avšak teprve v současné době byl prokázán jeho příznivý účinek v prevenci infarktu myokardu, cévní mozkové příhody, diabetes mellitus a hypertenze. Pití velmi dobře působí také v pokročilém věku. Nejlepší účinky má každodenní pití při večeři, u mužů 20–40 g alkoholu, u žen polovina této dávky., We have been drinking wine at least for 10 000 years or longer, in our region already from Celtic and Germanic times. Favorable effects on prevention of myocardial infarction, stroke, diabetes and hypertension were demonstrated recently, following attempts to use alcohol for treatment in ancient times. Favorable effects of wine drinking could be seen also in aging population. The best results for men are reached by daily drinking of 20–40 g alcohol at dinner. A moderate dose for women represents half of the dose for men., Milan Šamánek, Zuzana Urbanová, and Literatura 2
Rights:
http://creativecommons.org/publicdomain/mark/1.0/ and policy:public

37. Late blood pressure reduction in SHR subjected to transient captopril treatment in youth: possible mechanisms

Creator:
Josef Zicha, Zdena Dobešová, and Jiří Kuneš
Format:
print, bez média, and svazek
Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, fyziologie, genetika živočichů, hypertenze, physiology, animal genetics, hypertension, genetic hypertension, late effects of early treatment, captopril, nifedipine, 14, and 612
Language:
English
Description:
Spontaneously hypertensive rats (SHR) are characterized by enhanced nifedipine-sensitive component of sympathetic vasoconstriction. Our study tried to elucidate the mechanisms responsible for long-term reduction of blood pressure (BP) in SHR subjected to early transient captopril treatment. Adult untreated SHR aged 30-34 weeks were compared with animals subjected to chronic captopril treatment for 6 weeks either in youth (between 4 and 10 weeks of age) or in adulthood (between 24 and 30 weeks of age). Antihypertensive effects of captopril were more pronounced in young than adult SHR. This was due to greater attenuation of sympathetic and nifedipine-sensitive BP components and prevention of residual BP rise in young captopril-treated SHR in which the reductions of nifedipine-sensitive BP component and residual BP persisted for 20 weeks after captopril withdrawal. The magnitude of nifedipine-sensitive component of sympathetic vasoconstriction is decisive for BP maintenance not only in untreated SHR but also in SHR during active captopril treatment by or after its withdrawal., J. Zicha, Z. Dobešová,J. Kuneš., and Obsahuje bibliografii a bibliografické odkazy
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

38. Long-term administration of D-NAME induces hemodynamic and structural changes in the cardiovascular system

Creator:
Pavel Babál, Oľga Pecháňová, and Iveta Bernátová
Format:
print, bez média, and svazek
Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, hypertenze, hypertension, nitric oxide synthase, L-NAME, D-NAME, myocardial fibrosis, arterial hyperplasia, 14, and 612
Language:
English
Description:
NG-nitro-D-arginine-methyl ester (D-NAME) is considered to be an inactive enantiomer of L-NAME and is generally used as the negative control for NO synthase inhibition with L-NAME. With the aim to compare the effects of 4-week L-NAME and D-NAME treatments on hemodynamic and cardiovascular structural parameters, four groups of male Wistar rats were investigated: the controls and groups administered 40 and 20 mg/kg/day of L-NAME and 40 mg/kg/day of D-NAME. At the end of the experiment, myocardial NO synthase activity decreased by 42, 24 and 25 %; aortic NO synthase activity decreased by 35, 15 and 13 % vs. controls in the L-NAME 40, L-NAME 20 and D-NAME 40 groups, respectively. The DNA concentrations in the myocardium and the aorta increased significantly after L-NAME and D-NAME treatments. The inhibition of NO synthase was accompanied by a significant elevation in systolic blood pressure in all three groups. The LVW/BW ratio increased by 27, 14 and 13 % vs. controls in the L-NAME 40, L-NAME 20 and D-NAME 40 groups, respectively. The aortic wall mass, measured as the crossectional area, increased by 45, 17 and 25 % vs. controls in the L-NAME 40, L-NAME 20 and D-NAME 40 groups, respectively. Myocardial fibrosis represented 0.94 % in the controls, but 7.96, 4.70 and 5.25 % in L-NAME 40, L-NAME 20 and D-NAME 40 groups, respectively. It is concluded that D-NAME, although less affective than L-NAME, inhibits NO synthase activity resulting in hemodynamic and structural changes in the cardiovascular system similar to the changes induced by half the dose of L-NAME. Thus, the consideration of D-NAME as an inactive enantiomer and its use as the negative control needs to be reevaluated., P. Babál, O. Pecháňová, I. Bernátová., and Obsahuje bibliografii
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

39. Mechanismy vývinu hypertenze závislé na soli

Creator:
Michal Pravenec
Format:
print, bez média, and svazek
Type:
article, články, model:article, and TEXT
Subject:
Biologické vědy, hypertenze, kuchyňská sůl, hemodynamika, fyziologie, hypertension, table salt, hemodynamics, physiology, vliv soli, mineralokortikoidy, aldosteron, mineralocorticoids, 2, and 57/59
Language:
Czech
Description:
Hypertenze závislá na soli patří mezi nejčastější rizikové faktory kardiovaskulárních onemocnění. U většiny případů je příčina tohoto onemocnění neznámá, avšak významný podíl hypertenzních jedinců citlivých k soli má zvýšené hladiny mineralokortikoidů. V tomto přehledném článku popisujeme hemodynamické abnormality a mechanismy odpovědné za vývin této formy hypertenze., Salt-dependent hypertension is a leading cause of cardiovascular diseases. In most cases, the etiology is unknown, but it has been estimated that a significant percentage of salt-sensitive hypertensive individuals have mineralocorticoid excess. In this review, we describe hemodynamic abnormalities and mechanisms responsible for initiation of this form of hypertension., and Michal Pravenec.
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

40. Microalbuminuria versus brain natriuretic peptide in cardiac hypertrophy of hypertensive rats

Creator:
Saliba, Y., Chouery, E., Mégarbané, A., Jabbour, H., and Farès, N.
Format:
print, bez média, and svazek
Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, hypertenze, hypertension, microalbuminuria, brain natriuretic peptide, cardiac hypertrophy, 14, and 612
Language:
English
Description:
The objective of this study was to assess a possible link between microalbuminuria (MA), a major ri sk factor of the cardiorenal syndrome and the brain natriuretic peptide (BNP), a marker of cardiac hypertrophy. Two kidney-one clip (2K-1C) renovascular hypertension was induced in 24 male Wistar rats (weighing 220-250 g). Rats were randomized into four groups for 8 weeks: Sham, not treated; Bos, treated with bosentan; Cap, treated with captopril; Bos/Cap, treated with both drugs. Blood pressure, plasma BNP and transforming growth factor β1 (TGF-β1) concentrations, microalbuminuria and creatininemia as well as cardiac mass, BNP, α- and β-myosin heavy chain (MHC) gene expression and kidney histology were determined. Following stenosis, Sham rats developed hypertension (p<0.001), an increase in BNP (p<0.05) and TGF-β1 (p<0.005) concentrations, creatinine levels (p<0.001), and urinary albumin (p<0.001). Under drug treatment, decreases in blood pressure (p<0.001), creatinine levels (p<0.05), plasma TGF-β1 (p<0.005) and BNP (p<0.05) concentrations, were co ncomitant with the absence of MA which was significantly correlated with reductions in cardiac mass (p<0.05) and hypertrophy markers (BNP and β-MHC gene expression) (p<0.005) as well as in renal fibrosis. These findings suggest a potential link between microalbuminuria evolution and BNP as well as a possible effect of microalbuminuria-lowering therapy on halting the progression, or even inducing the regression of cardiac hypertrophy., Y. Saliba, E. Chouery, A. Mégarbané, H. Jabbour, N. Farès., and Obsahuje bibliografii
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public