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72. Restriction of nitric oxide rather than elevated blood pressure is responsible for alterations of vascular responses in nitric oxide-deficient hypertension
- Creator:
- Holécyová, A., Török, J., Bernátová, I., and Pecháňová, O.
- Type:
- article, model:article, and TEXT
- Subject:
- nitric oxide, L-NAME, hypertension, pulmonary and systemic vascular reactivity, and rat
- Language:
- English
- Description:
- The responsiveness of isolated high-pressure (aorta, renal artery) and low-pressure vessels (pulmonary artery) was compared during systemic hypertension induced by chronic inhibition of nitric oxide synthesis by NG-nitro-L-arginine methyl ester (L-NAME) in rats. L-NAME (40 mg/kg/day) was given to animals in their drinking water. After 4 weeks of L-NAME treatment, systolic blood pressure increased by 37 % as compared with that in the control group. Chronic L-NAME treatment resulted in significant reduction of endothelium-dependent relaxation to acetylcholine (10-8 to 3xl0-6 mol/1) in both types of vessels. The reduced relaxation was not influenced by acute pretreatment with indomethacin (10"5 mol/1), however, it was further reduced by acute pretreatment with additional L-NAME (10-4 mol/1). L-arginine (10-4 mol/1) improved the reduced relaxation. Endothelium- independent relaxation to sodium nitroprusside (10-9 to 10-6 mol/1) was unaffected by L-NAME treatment. /3-adrenoceptor-mediated relaxation to isoprénaline (10“8 to 3xl0-6 mol/1) was also not influenced by chronic L-NAME treatment Similar alterations in the responsiveness of high- and low- pressure vessels indicate rather the decisive role of nitric oxide restriction than that of elevated blood pressure in their development
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
73. Role of endothelium and nitric oxide in experimental hypertension
- Creator:
- Vapaatalo, H., Mervaala, E., and Nurminen, M.-L.
- Format:
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- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, endotel, endoteliální dysfunkce, oxid dusnatý, hypertenze, endothelium, endothelial dysfunction, nitric oxide, hypertension, antihypertensive drugs, 14, and 612
- Language:
- English
- Description:
- A short review on the role of endothelium and nitric oxide (NO) in experimental hypertension is presented in the light of the literature and our own recent findings. Based on these data, it is concluded that even though there is a lot of evidence in favor of the primary and causal association of endothelial dysfunction and NO in experimental hypertension, it seems still more plausible that they are causative in some types of hypertension only. Our own experience rather speaks for a secondary but still an important participation of endothelium in the maintenance and further elevation of high blood pressure. Endothelium plays a key role in the development of organ damages in hypertension., H. Vapaatalo, E. Mervaala, M.-L. Nurminen., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
74. Role of protoolysis and apoptosis in regression of pulmonary vascular remodeling
- Creator:
- Riley, D. J., Thakker-Varia, S., Wilson, F. J., Poiani, G. J., and Tozzi, C. A.
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- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, apoptóza, hypertenze, apoptosis, hypertension, vascular remodeling, matrix metalloproteinase, pulmonary, 14, and 612
- Language:
- English
- Description:
- Remodeled pulmonary arteries return to normal structural conditions after the increase in pulmonary artery flow resistance is reversed. We studied whether proteolysis of extracellular matrix proteins and apoptosis occur during reversal of remodeling produced by chronic hypoxia in the rat. Main pulmonary arteries were removed at different times during a 10-day period of exposure to 10% O2 and 14 days after return to air. Content and rates of degradation of collagen and elastin as well as immunoreactive collagenase in tissue and isolated mast cells were measured. Immunoblots for collagenase and tissue inhibitor of metalloproteinases (TIMP) were performed. Apoptosis was assessed by cleavage of DNA and TUNEL assay. Excess collagen and elastin present at 10 days of hypoxia decreased to near normal levels after 3-5 days of air. Transient increases in collagenolytic and elastolytic enzyme activities accompanied the rapid decrease in matrix proteins. Mast cells containing collagenase accumulated in remodeled pulmonary arteries, and the active form of collagenase appeared at the time of peak proteolytic activity. TIMP increased during remodeling. Apoptosis was maximal 3 days after return to air. Our results suggest that activation of enzymes, which degrade matrix proteins, and apoptosis play a role in resolution of vascular remodeling., D. J. Riley, S. Thakker-Varia, F. J. Wilson, G. J. Poiani, C. A. Tozzi., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
75. ROS production is increased in the kideny but not in the brain of dahl rats with salt hypertension elicited in adulthood
- Creator:
- Martina Vokurková, Hana Rauchová, Řezáčová, L., Ivana Vaněčková, and Josef Zicha
- Format:
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- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, hypertenze, fyziologie, hypertension, physiology, dahl rats, lipid peroxidation, nicotinamide-adenine dinucleotide phosphate (NADPT) oxidase, reactive oxygen species, salt hypertension, 14, and 612
- Language:
- English
- Description:
- Enhanced production of superoxide radicals by nicotinamideadenine dinucleotide phosphate (NADPH) oxidase in the brain and/or kidney of salt hypertensive Dahl rats has been proposed to participate in the pathogenesis of this form of experimental hypertension. Most information was obtained in young Dahl saltsensitive (DS) rats subjected to high salt intake prior to sexual maturation. Therefore, the aim of our study was to investigate whether salt hypertension induced in adult DS rats is also accompanied with a more pronounced oxidative stress in the brain or kidney as compared to Dahl salt-resistant (DR) controls. NADPH oxidase activity as well as the content of thiobarbituric acid-reactive substances (TBARS) and conjugated dienes (oxidative index), which indicate a degree of lipid peroxidation, were evaluated in two brain regions (containing either hypothalamic paraventricular nucleus or rostral ventrolateral medulla) as well as in renal medulla and cortex. High salt intake induced hypertension in DS rats but did not modify blood pressure in DR rats. DS and DR rats did not differ in NADPH oxidase-dependent production of ROS, TBARS content or oxidative index in either part of the brain. In addition, high-salt diet did not change significantly any of these brain parameters. In contrast, the enhanced NADPH oxidase-mediated ROS production (without significant signs of increased lipid peroxidation) was detected in the renal medulla of salt hypertensive DS rats. Our findings suggest that there are no signs of enhanced oxidative stress in the brain of adult Dahl rats with salt hypertension induced in adulthood., M. Vokurková, H. Rauchová, L. Řezáčová, I. Vaněčková, J. Zicha., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
76. Sex differences in blood pressure of aged Ren-2 transgenic rats
- Creator:
- Rauchová, Hana , Hojná, Silvie , Kadlecová, Michaela , Vaněčková, Ivana , and Zicha, Josef
- Format:
- počítač and online zdroj
- Type:
- model:article and TEXT
- Subject:
- hypertension, thiobarbituric acid-reactive species (TBARS), reduced glutathione, total plasma cholesterol, and HDL and LDL cholesterol fractions
- Language:
- English
- Description:
- Sex-related differences were observed not only in human but also in experimental hypertension. The aim of our study was to compare blood pressure (BP) of aged male and female heterozygous transgenic rats (TGR) harboring Ren-2 mouse gene, with their normotensive Hannover Sprague-Dawley (HanSD) controls. At the age of 9 months, systolic (SBP) and diastolic blood pressure (DBP) were measured by a direct puncture of carotid artery in rats awaking from isoflurane anesthesia. Thiobarbituric acid-reactive species (TBARS) formation was monitored as indicator of lipid peroxidation damage in heart, kidney and liver, whereas intracellular content of reduced glutathione was determined in the same organs as the main intracellular antioxidant. Furthermore, plasma triglycerides and total cholesterol as well as high-density lipoprotein (HDL) and low-density lipoprotein (LDL) fractions of cholesterol were measured. As compared to HanSD rats, we found significantly elevated BP only in male TGR (MAP: 123±1 vs. 171±5, SBP: 150±2 vs. 208±7, and DBP: 99±3 vs. 140±4 mm Hg), but not between TGR and HanSD females, which were both normotensive. We also did not find any significant differences in TBARS and reduced glutathione in the three above mentioned organs as well as in plasma cholesterol or its HDL and LDL fractions between transgene-negative HanSD and TGR animals of either sex. However, we found significant sex differences in TBARS, glutathione and plasma lipids in both rat strains. Our results confirmed that aged TGR exhibit a marked sexual BP dimorphism, which does not seem to be dependent on oxidative stress or abnormal cholesterol metabolism.
- Rights:
- http://creativecommons.org/publicdomain/mark/1.0/ and policy:public
77. Simvastatin decreased coenzyme Q in the left ventricle and skeletal muscle but not in the brain and liver in L-NAME-induced hypertension
- Creator:
- Jarmila Kucharská, Anna Gvozdjáková, and Fedor Šimko
- Format:
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- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, hypertenze, hypertension, simvastatin, NO-deficient hypertension, tissue coenzyme Q, L_NAME, 14, and 612
- Language:
- English
- Description:
- Inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase (statins) have been proven to reduce effectively cholesterol level and morbidity and mortality in patients with coronary heart disease and/or dyslipoproteinemia. Statins inhibit synthesis of mevalonate, a precursor of both cholesterol and coenzyme Q (CoQ). Inhibited biosynthesis of CoQ may be involved in some undesirable actions of statins. We investigated the effect of simvastatin on tissue CoQ concentrations in the rat model of NO-deficient hypertension induced by chronic L-NAME administration. Male Wistar rats were treated daily for 6 weeks with L-NAME (40 mg/kg) or with simvastatin (10 mg/kg), another group received simultaneously L-NAME and simvastatin in the same doses. Coenzyme Q9 and Q10 concentrations were analyzed by high performance liquid chromatography. L-NAME and simvastatin alone had no effect on CoQ concentrations. However, simultaneous application of L-NAME and simvastatin significantly decreased concentrations of both CoQ homologues in the left ventricle and slightly decreased CoQ9 concentration in the skeletal muscle. No effect was observed on CoQ level in the liver and brain. We conclude that the administration of simvastatin under the condition of NO-deficiency reduced the level of CoQ in the heart and skeletal muscle what may participate in adverse effect of statins under certain clinical conditions., J. Kucharská, A. Gvozdjáková, F. Šimko., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
78. Slow breathing training reduces resting blood pressure and the pressure responses to exercise
- Creator:
- Jones, C. U., Sangthong, B., Pachirat, O., and Jones, D. A.
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- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, hypertenze, srdeční rytmus, hypertension, heart rate, slow breathing training, muscle pressor response, heart rate variability, 14, and 612
- Language:
- English
- Description:
- Slow breathing training reduces resting blood pressure, probably by modifying central autonomic control, but evidence for this is lacking. The pressor response to static handgr ip exercise is a measure of autonomic control and the aim of this study was to determine whether slow breathing training modulates the pressor responses to exercise of untrained muscles. Twenty hypertensive patients trained for 8 weeks, 10 with unloaded slow breathing (Unloaded) and 10 breathing against an inspiratory load of 20 cm H 2 O (Loaded). Ten subjects were untrained controls. Subjects performed a 2 min handgrip pressor test (30 % MVC) pre - and post- training, and blood pressure and heart rate (HR) were measured before the contraction, at the end and following 2 min recovery. Resting systolic (sBP) and HR were reduced as a result of tra ining, as reported previously. After training there was both a smaller pressor response to hand grip exercise and a more rapid recovery of sBP and HR compared to pre -training. There were no changes in the Controls and no differences between the Unloaded and Loaded groups. Combining the two training groups, the sBP response to handgrip exercise after training was reduced by 10 mm Hg (95 % CI: - 7, - 13) and HR by 5 bpm (95 % CI: - 4, - 6), all p<0.05. These results are consistent with slow breathing training modifying central mechanisms regulating cardiovascular function., C. U. Jones, B. Sangthong, O. Pachirat, D. A. Jones., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
79. Spironolactone differently influences remodeling of the left ventricle and aorta in L-NAME-induced hypertension
- Creator:
- Fedor Šimko, Jana Matúšková, Ivan Ľupták, Terézia Pinčíková, Kristína Krajčírovičová, Svetoslav Štvrtina, Pomšár, J., Václav Pelouch, Ľudovít Paulis, and Oľga Pecháňová
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- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, hypertenze, oxid dusnatý, hypertension, nitric oxide, L-NAME, NO-deficient hypertension, spironolactone, left ventricular hypertrophy, aorta remodeling, 14, and 612
- Language:
- English
- Description:
- Aldosterone receptor antagonist, spironolactone, has been shown to prevent remodeling of the heart in several models of left ventricular hypertrophy. The aim of the present study was to determine whether the treatment with spironolactone can prevent hypertension, reduction of tissue nitric oxide synthase activity and left ventricular (LV) and aortic remodeling in NG-nitro-L-arginine methyl ester (L-NAME)-induced hypertension. Four groups of rats were investigated: control, spironolactone (200 mg/kg), L-NAME (40 mg/kg) and L-NAME + spironolactone (in corresponding dosage). Animals were studied after 5 weeks of treatment. The decrease of NO-synthase activity in the LV and kidney was associated with the development of hypertension and LV hypertrophy, with increased DNA concentration in the LV, and remodeling of the aorta in the L-NAME group. Spironolactone prevented the inhibition of NO-synthase activity in the LV and kidney and partially attenuated hypertension and LVH development and the increase in DNA concentration. However, remodeling of the aorta was not prevented by spironolactone treatment. We conclude that the aldosterone receptor antagonist spironolactone improved nitric oxide production and partially prevented hypertension and LVH development without preventing hypertrophy of the aorta in NO-deficient hypertension. The reactive growth of the heart and aorta seems to be controlled by different mechanisms in L-NAMEinduced hypertension., F. Šimko, J. Matúšková, I. L'upták, T. Pinčíková, K. Krajčírovičová, S. Štvrtina, J. Pomšár, V. Pelouch, L'. Paulis, O. Pecháňová., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
80. Spontaneous, L-arginine-induced and spironolactone-induced regression of protein remodeling of the left ventricle in L-NAME-induced hypertension
- Creator:
- Fedor Šimko, Anna Potáčová, Václav Pelouch, Ľudovít Paulis, Jana Matúšková, Kristína Krajčírovičová, Oľga Pecháňová, and Michaela Adamcová
- Format:
- print, bez média, and svazek
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, kolagen, hypertenze, collagen, hypertension, L_NAME hypertension, L-arginine, spironolactone, regression of hypertrophy, 14, and 612
- Language:
- English
- Description:
- NG-nitro-L-arginine-methyl ester (L-NAME)-induced hypertension is associated with protein remodeling of the left ventricle. The aim of the study was to show, whether aldosterone receptor blocker spironolactone and precursor of NOproduction L-arginine were able to reverse the protein rebuilding of the left ventricle. Six groups of male Wistar rats were investigated: control 4 (4 weeks placebo), L-NAME (4 weeks L-NAME), spontaneous-regression (4 weeks L-NAME + 3 weeks placebo), spironolactone-regression (4 weeks L-NAME + 3 weeks spironolactone), L-arginineregression (4 weeks L-NAME + 3 weeks arginine), control 7 (7 weeks placebo). L-NAME administration induced hypertension, hypertrophy of the left ventricle (LV), and the increase of metabolic and contractile as well as soluble and insoluble collagenous protein concentration. The systolic blood pressure and relative weight of the LV decreased in all three groups with regression, while the most prominent attenuation of the LVH was observed after spironolactone treatment. In the spontaneous-regression and L-arginine-regression groups the concentrations of individual proteins were not significantly different from the control value. However, in the spironolactone-regression group the concentration of metabolic, contractile and insoluble collagenous proteins remained significantly increased in comparison with the control group. The persistence of the increased protein concentration in the spironolactone group may be related to the more prominent reduction of myocardial water content by spironolactone., F. Šimko, A. Potáčová, V. Pelouch, L'. Paulis, J. Matúšková, K. Krajčírovičová, O. Pecháňová, M. Adamcová., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public