Exercise training (ET) is well established to induce vascular adaptations on the metabolically active muscles. These adaptations include increased function of vascular potassium channels and enhanced endothelium-dependent relaxations. However, the available data on the effect of ET on vasculatures that normally constrict during exercise, such as mesenteric arteries (MA), are scarce and not conclusive. Therefore, this study hypothesized that 10 weeks of moderate-intensity ET would result in adaptations towards more vasoconstriction or/and less vasodilatation of MA. Young Fischer 344 rats were randomly assigned to a sedentary group (SED; n=24) or exercise training group (EXE; n=28). The EXE rats underwent a progressive treadmill ET program for 10 weeks. Isometric tensions of small (SED; 252.9+/-29.5 microm, EXE; 248.6+/-34.4 microm) and large (SED; 397.7+/-85.3 microm, EXE; 414.0+/-86.95 microm) MA were recorded in response to cumulative phenylephrine concentrations (PE; 0-30 microM) in the presence and absence of the BKCa channel blocker, Iberiotoxin (100 nM). In another set of experiments, tensions in response to cumulative concentration-response curves of acetylcholine (ACh) or sodium nitroprusside (SNP) were obtained, and pEC50s were compared. Immunoblotting was performed to measure protein expression levels of the BKCa channel subunits and eNOS. ET did not alter the basal tension of small and large MA but significantly increased their responses to PE, and reduced the effect of BKCa channels in opposing the contractile responses to PE without changes in the protein expression level of BKCa subunits. ET also elicited a size-dependent functional adaptations that involved reduced endothelium-independent and endothelium-dependent relaxations. In large MA the sensitivity to SNP was decreased more than in small MA suggesting impaired nitric oxide (NO)-dependent mechanisms within the vascular smooth muscle cells of ET group. Whereas the shift in pEC50 of ACh-induced relaxation of small MA would suggest more effect on the production of NO within the endothelium, which is not changed in large MA of ET group. However, the eNOS protein expression level was not significantly changed between the ET and SED groups. In conclusion, our results indicate an increase in contraction and reduced relaxation of MA after 10 weeks of ET, an adaptation that may help shunt blood flow to metabolically active tissues during acute exercise.

• MeSH
• arteriae mesentericae MeSH
• cévní endotel metabolismus   MeSH
• krysa rodu rattus MeSH
• nitroprusid farmakologie   MeSH
• oxid dusnatý * metabolismus   MeSH
• vazodilatace * MeSH
• vazokonstrikce MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH

Being a chilling-sensitive staple crop, rice (Oryza sativa L.) is vulnerable to climate change. The competence of rice to withstand chilling stress should, therefore, be enhanced through technological tools. The present study employed chemical intervention like application of sodium nitroprusside (SNP) as nitric oxide (NO) donor and elucidated the underlying morpho-physiological and biochemical mechanisms of NO-mediated chilling tolerance in rice plants. At germination stage, germination indicators were interrupted by chilling stress (5.0 ± 1.0 °C for 8 h day-1), while pretreatment with 100 μM SNP markedly improved all the indicators. At seedling stage (14-day-old), chilling stress caused stunted growth with visible toxicity along with alteration of biochemical markers, for example, increase in oxidative stress markers (superoxide, hydrogen peroxide, and malondialdehyde) and osmolytes (total soluble sugar; proline and soluble protein content, SPC), and decrease in chlorophyll (Chl), relative water content (RWC), and antioxidants. However, NO application attenuated toxicity symptoms with improving growth attributes which might be related to enhance activities of antioxidants, mineral contents, Chl, RWC and SPC. Furthermore, principal component analysis indicated that water imbalance and increased oxidative damage were the main contributors to chilling injury, whereas NO-mediated mineral homeostasis and antioxidant defense were the critical determinants for chilling tolerance in rice. Collectively, our findings revealed that NO protects against chilling stress through valorizing cellular defense mechanisms, suggesting that exogenous application of NO could be a potential tool to evolve cold tolerance as well as climate resilience in rice.

• MeSH
• donory oxidu dusnatého farmakologie   MeSH
• homeostáza účinky léků   MeSH
• klíčení účinky léků   MeSH
• malondialdehyd metabolismus   MeSH
• nitroprusid farmakologie   MeSH
• nízká teplota MeSH
• ochrana úrody metody   MeSH
• oxid dusnatý metabolismus   MeSH
• peroxid vodíku metabolismus   MeSH
• peroxidace lipidů účinky léků   MeSH
• peroxidasy metabolismus   MeSH
• reakce na chladový šok fyziologie   MeSH
• rýže (rod) účinky léků   MeSH
• semenáček účinky léků   MeSH
• superoxidy metabolismus   MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

Nitric oxide (NO) is a major gasotransmitter involved in several physiological processes of male reproduction. There is, nevertheless, little information concerning the role of NO during semen storage. The aim of this study was to evaluate the effect of NO on boar semen stored at 17oC for 72 h. For this purporse, sperm samples were treated with 0.625, 1.25, 2.5, 5, and 10 mM aminoguanidine (AG) or Nω-Nitro-L-arginine methyl ester hydrochloride (L-NAME), a selective and non-selective NO synthase (NOS) inhibitor, respectively. Moreover, sodium nitroprusside (SNP), a NO donor, was used at the dose of 18.75, 37.5, 75, and 150 μM. Sperm motility, membrane integrity, and acrosomal status were evaluated at 0, 4, 24, 48, and 72 h of semen storage. A significant increase of the amplitude of lateral sperm head displacement (ALH), and both curvilinear and straight-line velocity (VCL and VSL, respectively) was observed at 72 h of semen storage in samples treated with 0.625 mM AG, probably because of the antioxidant properties of this NOS inhibitor. Contrarily, 0.625 mM L-NAME showed no effect on boar sperm parameters during the entire period of semen storage. Moreover, AG and L-NAME at 10 mM negatively affected sperm kinetics and acrosome integrity, which may provide further support to the notion that low NO levels are necessary for a normal sperm function. The concentrations of SNP used in this study had mostly no or negative effects on boar sperm parameters during semen storage. In conclusion, the results from this study increase the understanding of the role of NO on boar sperm physiology.

• MeSH
• akrozom účinky léků   MeSH
• buněčná membrána účinky léků   MeSH
• časové faktory MeSH
• guanidiny farmakologie   MeSH
• motilita spermií účinky léků   MeSH
• nitroprusid farmakologie   MeSH
• oxid dusnatý aplikace a dávkování   farmakologie   MeSH
• prasata * MeSH
• spermie účinky léků   MeSH
• synthasa oxidu dusnatého, typ II antagonisté a inhibitory   metabolismus   MeSH
• uchování spermatu veterinární   MeSH
• zvířata MeSH
• Check Tag
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH

The endothelial barrier function is tightly controlled by a broad range of signaling cascades including nitric oxide-cyclic guanosine monophosphate (NO-cGMP) pathway. It has been proposed that disturbances in NO and cGMP production could interfere with proper endothelial barrier function. In this study, we assessed the effect of interferon-gamma (IFN-gamma), a pro-inflammatory cytokine, on NO and cGMP levels and examined the mechanisms by which NO and cGMP regulate the IFN-gamma-mediated HUVECs hyperpermeability. The flux of fluorescein isothiocyanate-labeled dextran across cell monolayers was used to study the permeability of endothelial cells. Here, we found that IFN-gamma significantly attenuated basal NO concentration and the increased NO levels supplied by a NO donor, sodium nitroprusside (SNP). Besides, application of IFN-gamma also significantly attenuated both the basal cGMP concentration and the increased cGMP production donated by a cell permeable cGMP analogue, 8-bromo-cyclic GMP (8-Br-cGMP). In addition, exposure of the cell monolayer to IFN-gamma significantly increased HUVECs basal permeability. However, L-NAME pretreatment did not suppress IFN-gamma-induced HUVECs hyperpermeability. L-NAME pretreatment followed by SNP or SNP pretreatment partially reduced IFN-gamma-induced HUVECs hyperpermeability. Pretreatment with a guanylate cyclase inhibitor, 6-anilino-5,8-quinolinedione (LY83583), led to a further increase in IFN-gamma-induced HUVECs hyperpermeability. The findings suggest that the mechanism underlying IFN-gamma-induced increased HUVECs permeability is partly related to the inhibition of NO production.

• MeSH
• donory oxidu dusnatého farmakologie   MeSH
• endoteliální buňky pupečníkové žíly (lidské) účinky léků   metabolismus   MeSH
• guanosinmonofosfát cyklický analogy a deriváty   metabolismus   farmakologie   MeSH
• guanylátcyklasa antagonisté a inhibitory   MeSH
• inhibitory enzymů farmakologie   MeSH
• interferon gama farmakologie   MeSH
• kapilární permeabilita účinky léků   MeSH
• lidé MeSH
• NG-nitroargininmethylester farmakologie   MeSH
• nitroprusid farmakologie   MeSH
• oxid dusnatý metabolismus   MeSH
• permeabilita buněčné membrány MeSH
• Check Tag
• lidé MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH

Causes of early hypoperfusion after subarachnoid hemorrhage (SAH) include intracranial hypertension as well as vasoconstriction. The aim of the study was to assess the effect of intracerebroventricular (ICV) administration of sodium nitroprusside (SNP) on early hypoperfusion after SAH. Male Wistar rats (220-240 g) were used, SAH group received 250 microl of fresh autologous arterial blood into the prechiasmatic cistern; sham-operated animals received 250 microl of isotonic solution. Therapeutic intervention: ICV administration of 10 microg SNP; 5 microl 5 % glucose (SNP vehicle) and untreated control. Brain perfusion and invasive blood pressure were monitored for 30 min during and after induction of SAH. Despite SNP caused increase of perfusion in sham-operated animals, no response was observed in half of SAH animals. The other half developed hypotension accompanied by brain hypoperfusion. There was no difference between brain perfusion in SNP-treated, glucose-treated and untreated SAH animals during the monitored period. We did not observe expected beneficial effect of ICV administration of SNP after SAH. Moreover, half of the SNP-treated animals developed serious hypotension which led to brain hypoperfusion. This is the important finding showing that this is not the option for early management in patient after SAH.

• MeSH
• antihypertenziva aplikace a dávkování   škodlivé účinky   MeSH
• intrakraniální hypotenze chemicky indukované   patofyziologie   MeSH
• intraventrikulární infuze MeSH
• krysa rodu rattus MeSH
• mozek krevní zásobení   účinky léků   patofyziologie   MeSH
• mozkový krevní oběh účinky léků   fyziologie   MeSH
• nitroprusid aplikace a dávkování   škodlivé účinky   MeSH
• potkani Wistar MeSH
• subarachnoidální krvácení farmakoterapie   patofyziologie   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH

Vasospasm induced by nontraumatic subarachnoid bleeding is an important cause of ischaemic neurological damage among patients sustaining aneurysmal subarachnoid haemorrhage. Pathophysiology of this process is not fully understood. Apart from endovascular or surgical interventions, pharmacotherapy is currently used in clinical practice, using vasodilatory agents with various mechanism of action, routes of administration and timing. the efficacy of these interventions is uncertain and requires more experimental testing. In this project, a laboratory rat model of subarachnoid bleeding and early vasospasm will be created. Efficacy of intrathecal administration of vasodilatory agents and / or antioxidant (reducing risk of further brain damage by free radicals) will be tested. Furthermore, behavioral testing of changes of memory and motor functions and their correlation to pharmacologic interventions will be performed.

Vznik vazospazmu vyvolaného neutraumatickým subarachnoidální krvácením je vedoucí příčinou vzniku neurologického ischemického postižení u cca jedné čtvrtiny pacientů se SAK. Tento jev souvisí se strukturálními a biochemickými změnami na úrovni vaskulárního endotelu a buněk hladké svaloviny, které jsou navozeny hemoragií. Kromě endovaskulárních či chirurgických intervencí se i nadále ve farmakoterapii uplatňují vazodilatátory různého mechanismu účinku, různé cesty aplikace i načasování. Jejich účinnost je však nadále v klinické praxi sporná a vyžaduje experimentální ověření. Cílem projektu je vypracovat u laboratorních potkanů model subarachnoidálního krvácení a časného vazospazmu. Na modelu budeme testovat účinnost intrathekální aplikace vazodilatačních látek a / nebo aplikace antioxidantu snižujícího riziko poškození mozku volnými radikály. Dále budeme behaviorálně testovat změny paměti a motoriky a jejich závislost na farmakologické intervenci.

• MeSH
• antioxidancia aplikace a dávkování   MeSH
• arginin MeSH
• intrakraniální vazospazmus MeSH
• ischemie mozku MeSH
• krysa rodu rattus MeSH
• melatonin MeSH
• mozkový krevní oběh MeSH
• neurobehaviorální symptomy účinky léků   MeSH
• nitroprusid MeSH
• subarachnoidální krvácení MeSH
• vazodilatancia aplikace a dávkování   MeSH
• Check Tag
• krysa rodu rattus MeSH

• Konspekt
• Patologie. Klinická medicína
• NLK Obory
• neurologie
• NLK Publikační typ
• závěrečné zprávy o řešení grantu IGA MZ ČR

STR/N is an inbred strain of mice which is known to exhibit extreme polydipsia and polyuria. We previously found central administration of angiotensin II enhanced cardiovascular responses in STR/N mice than normal mice, suggesting that STR/N mice might exhibit different cardiovascular responses. Therefore, in this study, we investigated daily mean arterial blood pressure and heart rate, and changes in the baroreceptor-heart rate reflex in conscious STR/N mice and control (ICR) mice. We found that variability in daily mean arterial blood pressure and heart rate was significantly larger in STR/N mice than in ICR mice (p<0.05). There was a stronger response to phenylephrine (PE) in STR/N mice than in ICR mice. For baroreceptor reflex sensitivity, in the rapid response period, the slopes of PE and sodium nitroprusside (SNP) were more negative in STR/N mice than in ICR mice. In the later period, the slopes of PE and SNP were negatively correlated between heart rate and blood pressure in ICR mice, but their slopes were positively correlated in STR/N mice. These results indicated that STR/N mice exhibited the different cardiovascular responses than ICR mice, suggesting that the dysfunction of baroreceptor reflex happened in conscious STR/N mice.

• MeSH
• baroreflex účinky léků   MeSH
• fenylefrin farmakologie   MeSH
• krevní tlak MeSH
• myši inbrední ICR MeSH
• myši MeSH
• nitroprusid farmakologie   MeSH
• polydipsie genetika   patofyziologie   MeSH
• presoreceptory patofyziologie   MeSH
• srdeční frekvence * účinky léků   MeSH
• vazodilatancia farmakologie   MeSH
• vazokonstriktory farmakologie   MeSH
• zvířata MeSH
• Check Tag
• mužské pohlaví MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

Overproduction of reactive oxygen species (ROS) has been implicated in a range of pathologies. Mitochondrial flavin dehydrogenases glycerol-3-phosphate dehydrogenase (mGPDH) and succinate dehydrogenase (SDH) represent important ROS source, but the mechanism of electron leak is still poorly understood. To investigate the ROS production by the isolated dehydrogenases, we used brown adipose tissue mitochondria solubilized by digitonin as a model. Enzyme activity measurements and hydrogen peroxide production studies by Amplex Red fluorescence, and luminol luminescence in combination with oxygraphy revealed flavin as the most likely source of electron leak in SDH under in vivo conditions, while we propose coenzyme Q as the site of ROS production in the case of mGPDH. Distinct mechanism of ROS production by the two dehydrogenases is also apparent from induction of ROS generation by ferricyanide which is unique for mGPDH. Furthermore, using native electrophoretic systems, we demonstrated that mGPDH associates into homooligomers as well as high molecular weight supercomplexes, which represent native forms of mGPDH in the membrane. By this approach, we also directly demonstrated that isolated mGPDH itself as well as its supramolecular assemblies are all capable of ROS production.

• MeSH
• ferrikyanidy metabolismus   MeSH
• glycerolfosfátdehydrogenasa chemie   metabolismus   MeSH
• glycerolfosfáty metabolismus   MeSH
• krysa rodu rattus MeSH
• mitochondrie enzymologie   metabolismus   MeSH
• peroxid vodíku metabolismus   MeSH
• reaktivní formy kyslíku metabolismus   MeSH
• savci MeSH
• sukcinátdehydrogenasa chemie   metabolismus   MeSH
• transport elektronů * MeSH
• ubichinon metabolismus   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

Various nitric oxide modulators (NO donors--SNP, GSNO, DEA NONOate and scavengers--PTIO, cPTIO) were tested to highlight the role of NO under Cd excess in various ontogenetic stages of chamomile (Matricaria chamomilla). Surprisingly, compared to Cd alone, SNP and PTIO elevated Cd uptake (confirmed also by PhenGreen staining) but depleted glutathione (partially ascorbic acid) and phytochelatins PC2 and PC3 in both older plants (cultured hydroponically) and seedlings (cultured in deionised water). Despite these anomalous impacts, fluorescence staining of NO and ROS confirmed predictable assumptions and revealed reciprocal changes (decrease in NO but increase in ROS after PTIO addition and the opposite after SNP application). Subsequent tests using alternative modulators and seedlings confirmed changes to NO and ROS after application of GSNO and DEA NONOate as mentioned above for SNP while cPTIO altered only NO level (depletion). On the contrary to SNP and PTIO, GSNO, DEA NONOate and cPTIO did not elevate Cd content and phytochelatins (PC2, PC3) were rather elevated. These data provide evidence that various NO modulators are useful in terms of NO and ROS manipulation but interactions with intact plants affect metal uptake and must therefore be used with caution. In this view, cPTIO and DEA NONOate revealed the less pronounced side impacts and are recommended as suitable NO scavenger/donor in plant physiological studies under Cd excess.

• MeSH
• antioxidancia chemie   MeSH
• cyklické N-oxidy chemie   MeSH
• donory oxidu dusnatého chemie   MeSH
• fluorescenční mikroskopie MeSH
• glutathion chemie   MeSH
• heřmánek, heřmánkovec, rmen, rmenec účinky léků   MeSH
• imidazoly chemie   MeSH
• kadmium chemie   MeSH
• konfokální mikroskopie MeSH
• kyselina askorbová chemie   MeSH
• nitroprusid chemie   MeSH
• oxid dusnatý chemie   MeSH
• reaktivní formy kyslíku chemie   MeSH
• S-nitrosoglutathion chemie   MeSH
• semena rostlinná účinky léků   MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

• Klíčová slova
• akutní srdeční selhání, LEVOSIMENDAN, kalciové senzitizéry,
• MeSH
• digoxin terapeutické užití   MeSH
• diuretika terapeutické užití   MeSH
• dobutamin terapeutické užití   MeSH
• dopamin terapeutické užití   MeSH
• inhibitory fosfodiesterasy 3 terapeutické užití   MeSH
• kardiogenní šok * diagnóza   patofyziologie   terapie   MeSH
• kardiorenální syndrom farmakoterapie   MeSH
• lidé MeSH
• natriuretický peptid typu B terapeutické užití   MeSH
• neinvazivní ventilace metody   MeSH
• nitroglycerin terapeutické užití   MeSH
• nitroprusid terapeutické užití   MeSH
• srdeční selhání diagnóza   etiologie   farmakoterapie   komplikace   patofyziologie   terapie   MeSH
• vazodilatancia terapeutické užití   MeSH
• vazokonstriktory terapeutické užití   MeSH
• Check Tag
• lidé MeSH