• MeSH
• kosti a kostní tkáň krevní zásobení   MeSH
• krysa rodu rattus MeSH
• oxid dusnatý MeSH
• oxid dusný MeSH
• rychlost toku krve MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• ženské pohlaví MeSH
• zvířata MeSH

EDRF-NO probably participates-besides the prostaglandins [3, 4]-in local circulatory changes in the bones of female rats with modified level of sex hormones; we could demonstrate it indirectly using methylene blue as a blocking agent [5]. In this paper, we present corresponding results of two experiments with NG-nitro-arginine methyl ester (L-NAME) as a substance blocking the production of endothelium derived relaxing factor, i.e. nitric oxide (EDRF-NO). Circulatory values were estimated by means of 85Sr-microspheres. In experiment A we ascertained whether the duration of L-NAME administration (0.025% in the food) influenced the effect. It could be demonstrated that the effect of one week's, two weeks', or four weeks' administration of L-NAME was the same: 85Sr-microsphere uptake and blood flow throught the tibia of female rats, increased after oophorectomy (OOX, performed four weeks prior to the experiment), was significantly suppressed to the level in sham-operated animals. In the experiment B, L-NAME was administered in the food in concentration of 0.05% for two weeks prior to the experiment. 85Sr-microsphere uptake was decreased significantly after L-NAME in the tibia of sham-operated females, in the tibia and distal femur of OOX animals; no significant changes were found in the diaphysis of femur and in calvaria. Blood flow values were significantly decreased in all bone samples of OOX females and in tibia of sham-operated rats (besides the local reaction also due to the decrease in the cardiac output). In both experiments the cardiac output was decreased and blood pressure elevated after L-NAME. It can be concluded, from the results of both experiments, that the blockade of EDRF-NO production by L-NAME decreases local circulatory values in the bones of female rats-particularly OOX-in a similar way as methylene blue; however, in contrast to methylene blue, L-NAME induces marked increase in the blood pressure and partially decrease in the cardiac output. Thus, as in the case of methylene blue, the effect of L-NAME on the circulation of blood in the rat bones supports the hypothesis of the participation of EDRF-NO in bone blood flow regulations.

• MeSH
• femur krevní zásobení   MeSH
• hemodynamika účinky léků   MeSH
• kosti a kostní tkáň krevní zásobení   MeSH
• krysa rodu rattus MeSH
• methylenová modř farmakologie   MeSH
• NG-nitroargininmethylester farmakologie   MeSH
• ovarektomie MeSH
• oxid dusnatý antagonisté a inhibitory   biosyntéza   fyziologie   MeSH
• radioizotopy stroncia MeSH
• regionální krevní průtok účinky léků   MeSH
• rychlost toku krve účinky léků   MeSH
• tibie krevní zásobení   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• anglický abstrakt MeSH
• časopisecké články MeSH
• práce podpořená grantem MeSH

• MeSH
• corpus striatum krevní zásobení   MeSH
• ischemie mozku * patologie   MeSH
• lidé MeSH
• NG-nitroargininmethylester antagonisté a inhibitory   MeSH
• potkani Wistar MeSH
• receptory N-methyl-D-aspartátu biosyntéza   MeSH
• spektrofotometrie MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• abstrakty MeSH
• práce podpořená grantem MeSH

The renin-angiotensin-aldosterone system (RAAS) is a dominant player in several cardiovascular pathologies. This study investigated whether alterations induced by l-NAME, (NLG)-nitro-l-arginine methyl ester, a nitric oxide synthase inhibitor, and the protective effect of melatonin are associated with changes in the RAAS. Four groups of 3-month-old male Wistar rats (n = 10) were treated as follows for four weeks: untreated controls, rats treated with melatonin (10 mg/kg/day), rats treated with l-NAME (40 mg/kg/day), and rats treated with l-NAME + melatonin. l-NAME administration led to hypertension and left ventricular (LV) fibrosis in terms of enhancement of soluble, insoluble and total collagen concentration and content. Melatonin reduced systolic blood pressure enhancement and lowered the concentration and content of insoluble and total collagen in the LV. The serum concentration of angiotensin (Ang) 1-8 (Ang II) and its downstream metabolites were reduced in the l-NAME group and remained unaltered by melatonin. The serum aldosterone level and its ratio to Ang II (AA2-ratio) were increased in the l-NAME group without being modified by melatonin. We conclude that l-NAME-hypertension is associated with reduced level of Ang II and its downstream metabolites and increased aldosterone concentration and AA2-ratio. Melatonin exerts its protective effect in l-NAME-induced hypertension without affecting RAAS.

• MeSH
• hypertenze * chemicky indukované   metabolismus   patofyziologie   prevence a kontrola   MeSH
• krevní tlak účinky léků   MeSH
• krysa rodu rattus MeSH
• melatonin farmakologie   MeSH
• NG-nitroargininmethylester škodlivé účinky   farmakologie   MeSH
• potkani Wistar MeSH
• renin-angiotensin systém účinky léků   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH

High blood pressure (BP) of L-NAME hypertensive rats is maintained not only by the absence of nitric oxide (NO)- dependent vasodilatation but also by the enhancement of both sympathetic and angiotensin II-dependent vasoconstriction. The aim of the present study was to evaluate the role of inhibitory G (Gi) proteins, which are involved in tonic sympathetic vasoconstriction, in the pathogenesis of NO-deficient hypertension. We therefore studied BP response to chronic L-NAME administration (60 mg/kg/day for 4 weeks) in rats in which the in vivo inactivation of Gi proteins was induced by injection of pertussis toxin (PTX, 10 µg/kg i.v.). The impairment of sympathetic vasoconstriction due to PTX-induced Gi protein inactivation prevents the full development of NO-deficient hypertension because BP of PTX-treated rats subjected to chronic L-NAME administration did not reach hypertensive values. Nevertheless, chronic NO synthase inhibition per se is capable to increase moderately BP even in PTX-treated rats. Our data suggest that the sympathetic vasoconstriction is essential for the development of established NO-deficient hypertension.

• MeSH
• financování organizované MeSH
• hypertenze chemicky indukované   metabolismus   MeSH
• krysa rodu rattus MeSH
• modely nemocí na zvířatech MeSH
• NG-nitroargininmethylester MeSH
• pertusový toxin MeSH
• potkani Wistar MeSH
• proteiny vázající GTP - alfa-podjednotky Gi-Go antagonisté a inhibitory   metabolismus   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH

The aim of this study was to investigate nitric oxide (NO) production and L-NAME-sensitive component of endothelium-dependent vasorelaxation in adult normotensive Wistar-Kyoto rats (WKY), borderline hypertensive rats (BHR) and spontaneously hypertensive rats (SHR). Blood pressure (BP) of WKY, BHR and SHR (determined by tail-cuff) was 111+/-3, 140+/-4 and 184+/-6 mm Hg, respectively. NO synthase activity (determined by conversion of [(3)H]-L-arginine) was significantly higher in the aorta of BHR and SHR vs. WKY and in the left ventricle of SHR vs. both BHR and WKY. L-NAME-sensitive component of endothelium-dependent relaxation was investigated in the preconstricted femoral arteries using the wire myograph during isometric conditions as a difference between acetylcholine-induced relaxation before and after acute N(G)-nitro-L-arginine methyl ester pre-treatment (L-NAME, 10(-5) mol/l). Acetylcholine-induced vasorelaxation of SHR was significantly greater than that in WKY. L-NAME-sensitive component of vasorelaxation in WKY, BHR and SHR was 20+/-3 %, 29+/-4 % (p<0.05 vs. WKY) and 37+/-3 % (p<0.05 vs. BHR), respectively. There was a significant positive correlation between BP and L-NAME-sensitive component of relaxation of the femoral artery. In conclusion, results suggest the absence of endothelial dysfunction in the femoral artery of adult borderline and spontaneously hypertensive rats and gradual elevation of L-NAME-sensitive component of vasorelaxation with increasing blood pressure.

• MeSH
• acetylcholin farmakologie   MeSH
• aorta účinky léků   enzymologie   MeSH
• arteria femoralis účinky léků   patofyziologie   MeSH
• hypertenze genetika   metabolismus   patofyziologie   MeSH
• inhibitory enzymů farmakologie   MeSH
• krevní tlak * MeSH
• krysa rodu rattus MeSH
• modely nemocí na zvířatech MeSH
• NG-nitroargininmethylester farmakologie   MeSH
• oxid dusnatý metabolismus   MeSH
• potkani inbrední SHR MeSH
• potkani inbrední WKY MeSH
• srdeční komory účinky léků   enzymologie   MeSH
• stupeň závažnosti nemoci MeSH
• synthasa oxidu dusnatého antagonisté a inhibitory   metabolismus   MeSH
• vazodilatace účinky léků   MeSH
• vazodilatancia farmakologie   MeSH
• vztah mezi dávkou a účinkem léčiva MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

Red wine polyphenols have been reported to possess beneficial properties for preventing cardiovascular diseases but their neuroprotective effects during chronic L-NAME treatment have not been elucidated. The aim of this study was to analyze a time course of Provinols effects on brain NO synthase activity and oxidative damage in L-NAME-induced hypertension. Male Wistar rats, 12 weeks old, were divided into six groups: control groups, groups treated with N(G)-nitro-L-arginine methyl ester (L-NAME, 40 mg/kg/day) for 4 or 7 weeks and groups receiving Provinols (40 mg/kg/day) plus L-NAME for 4 or 7 weeks. At the end of the treatment, marker of membrane oxidative damage - conjugated dienes (CD) in the brain and NO synthase activity in the cerebral cortex, cerebellum and brainstem were determined. L-NAME treatment for 4 or 7 weeks led to the increase in blood pressure, elevation of CD concentration and decrease of NO synthase activity in the brain parts investigated. Provinols partially prevented blood pressure rise and elevation of CD concentration. Comparing to the L-NAME treated group, Provinols increased NO synthase activity after 4 weeks of treatment. However, the prolonged Provinols treatment for 7 weeks had no effect on NO synthase activity decreased by L-NAME treatment. In conclusion, Provinols partially prevents L-NAME induced hypertension via the different mechanisms depending on the duration of treatment. Prevention of oxidative damage in the brain with modulating effect on NO synthase activity is suggested.

• MeSH
• fenoly farmakologie   MeSH
• flavonoidy farmakologie   MeSH
• hypertenze chemicky indukované   enzymologie   MeSH
• krevní tlak účinky léků   MeSH
• krysa rodu rattus MeSH
• mozek účinky léků   enzymologie   MeSH
• neuroprotektivní látky farmakologie   MeSH
• NG-nitroargininmethylester MeSH
• oxidační stres MeSH
• polyfenoly MeSH
• potkani Wistar MeSH
• synthasa oxidu dusnatého metabolismus   MeSH
• víno * MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

Hypertension due to chronic inhibition of NO synthase (NOS) by Nomega-nitro-L-arginine methyl ester (L-NAME) administration is characterized by both impaired NO-dependent vasodilation and enhanced sympathetic vasoconstriction. The aim of our study was to evaluate changes in the participation of major vasoactive systems in L-NAME-treated rats which were subjected to simultaneous antihypertensive (captopril) or antioxidant (N-acetylcysteine, NAC) treatment. Three-month-old Wistar males treated with L-NAME (60 mg/kg/day) for 5 weeks were compared to rats in which L-NAME treatment was combined with simultaneous chronic administration of captopril or NAC. Basal blood pressure (BP) and its acute responses to consecutive i.v. injections of captopril (10 mg/kg), pentolinium (5 mg/kg), L-NAME (30 mg/kg), tetraethylammonium (TEA, 16 mg/kg) and nitroprusside (NP, 20 microg/kg) were determined in conscious rats at the end of the study. The development of L-NAME hypertension was prevented by captopril treatment, whereas NAC treatment caused only a moderate BP reduction. Captopril treatment normalized the sympathetic BP component and significantly reduced residual BP (measured at full NP-induced vasodilation). In contrast, chronic NAC treatment did not modify the sympathetic BP component or residual BP, but significantly enhanced NO-dependent vasodilation. Neither captopril nor NAC treatment influenced the compensatory increase of TEA-sensitive vasodilation mediated by endothelium-derived hyperpolarizing factor in L-NAME-treated rats. Chronic captopril treatment prevented L-NAME hypertension by lowering of sympathetic tone, whereas chronic NAC treatment attenuated L-NAME hypertension by reduction in the vasodilator deficit due to enhanced NO-dependent vasodilation.

• MeSH
• acetylcystein farmakologie   terapeutické užití   MeSH
• antihypertenziva farmakologie   terapeutické užití   MeSH
• hypertenze chemicky indukované   prevence a kontrola   MeSH
• kaptopril farmakologie   terapeutické užití   MeSH
• krevní tlak účinky léků   MeSH
• krysa rodu rattus MeSH
• NG-nitroargininmethylester antagonisté a inhibitory   farmakologie   MeSH
• nitroprusid farmakologie   terapeutické užití   MeSH
• pentoliniumtartrát farmakologie   terapeutické užití   MeSH
• potkani Wistar MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• práce podpořená grantem MeSH

N(G)-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 NO-production 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-arginine-regression (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.

• MeSH
• antagonisté mineralokortikoidních receptorů farmakologie   terapeutické užití   MeSH
• arginin farmakologie   terapeutické užití   MeSH
• hypertenze chemicky indukované   komplikace   farmakoterapie   metabolismus   patofyziologie   MeSH
• hypertrofie levé komory srdeční farmakoterapie   etiologie   metabolismus   patofyziologie   MeSH
• kolagen metabolismus   MeSH
• krevní tlak účinky léků   MeSH
• krysa rodu rattus MeSH
• myokard metabolismus   patologie   MeSH
• NG-nitroargininmethylester MeSH
• oxid dusnatý metabolismus   MeSH
• potkani Wistar MeSH
• remodelace komor účinky léků   MeSH
• spironolakton farmakologie   terapeutické užití   MeSH
• spontánní remise MeSH
• svalové proteiny metabolismus   MeSH
• velikost orgánu účinky léků   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

• MeSH
• fibróza etiologie   metabolismus   patologie   MeSH
• hypertrofie levé komory srdeční metabolismus   patologie   MeSH
• kolagen analýza   metabolismus   MeSH
• krysa rodu rattus MeSH
• NG-nitroargininmethylester farmakologie   MeSH
• oxid dusnatý nedostatek   MeSH
• synthasa oxidu dusnatého antagonisté a inhibitory   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• zvířata MeSH
• Publikační typ
• srovnávací studie MeSH