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52. Nitric oxide synthase in pulmonary hypertension: lessons from knockout mice
- Creator:
- Fagan, K. A., McMurtry, I., and Rodman, D. M.
- Format:
- print, bez média, and svazek
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, oxid dusnatý, plicní hypertenze, nitric oxide, pulmonary hypertension, knockout mice, pulmonary vasoreactivity, vascular remodeling, 14, and 612
- Language:
- English
- Description:
- Nitric oxide (NO) is implicated in a wide variety of biological roles. NO is generated from three nitric oxide synthase (NOS) isoforms: neuronal (nNOS), inducible (iNOS), and endothelial (eNOS) all of which are found in the lung. While there are no isoform-specific inhibitors of NOS, the recent development and characterization of mice deficient in each of the NOS isoforms has allowed for more comprehensive study of the importance of NO in the lung circulation. Studies in the mouse have identified the role of NO from eNOS in modulating pulmonary vascular tone and in attenuating the development of chronic hypoxic pulmonary hypertension., K. A. Fagan, I. McMurtry, D. M. Rodman., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
53. Non-quantal acetylcholine release at the neuromuscular junction
- Creator:
- František Vyskočil, Malomouzh, A. I., and Nikolsky, E. E.
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, fyziologie, acetylcholin, synapse, oxid dusnatý, hibernace, physiology, acetylcholine, synapses, nitric oxide, hibernation, non-quantal release, neuromuscular junction, desensitization, resting membrane potential, choline transporter, vesicular ACh transporter, anticholinesterase, N-acetylaspartylglutamate, miniature endplate potential, 14, and 612
- Language:
- English
- Description:
- There are two principal mechanisms of acetylcholine (ACh) release from the resting motor nerve terminal: quantal and non-quantal (NQR); the former being only a small fraction of the total, at least at rest. In the present article we summarize basic research about the NQR that is undoubtedly an important trophic factor during endplate development and in adult neuromuscular contacts. NQR helps to eliminate the polyneural innervation of developing muscle fibers, ensures higher excitability of the adult subsynaptic membrane by surplus polarization and protects the RMP from depolarization by regulating the NO cascade and chloride transport. It shortens the endplate potentials by promoting postsynaptic receptor desensitization when AChE is inhibited during anti-AChE poisoning. In adult synapses, it can also activate the electrogenic Na+/K+-pump, change the degree of synchronization of quanta released by the nerve stimulation and affects the contractility of skeletal muscles., F. Vyskočil, A. I. Malomouzh, E. E. Nikolsky., and Obsahuje seznam literatury
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
54. Opposite effects of nitric oxide on identified inhibitory and excitatory cholinergic synapses of aplysia californica
- Creator:
- Mothet, J. P., Fossier, P., Schirar, A., Tauc, L., and Baux, G.
- Type:
- article, model:article, and TEXT
- Subject:
- nitric oxide, guanylate cyclase, synaptic transmission, and voltage-gated presynaptic currents
- Language:
- English
- Description:
- The effects of nitric oxide on evoked acetylcholine (ACh) release were studied at two identified cholinergic neuro-neuronal synapses of the nervous system of the mollusc Aplysia californica. The NO- donor, 3-morpholinosydnonimine (SIN-1), decreased the amplitude of evoked inhibitory postsynaptic currents (buccal ganglion) and potentiated that of evoked excitatory postsynaptic currents (abdominal ganglion). SIN-1 acted by modulating the number of ACh quanta released. 8Br-cGMP mimicked the effects of NO on ACh release in both types of synapses thus pointing to the involvement of a NO- sensitive guanylate cyclase. Presynaptic voltage-dependent Ca2+ and K+ (Ia and late outward rectifier) currents were not modified by SIN-1 suggesting another final target for NO/cGMP. The labelling of a NO-synthase by immunostaining in several neurones as well as the modulation of ACh release by L-arginine indicate that an endogenous NO-synthase is involved in the modulation of synaptic efficacy in both buccal and abdominal ganglia.
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
55. Oral administration of polyphenolic compounds from Cognac decreases ADP-induced platelet aggregation and reduces chronotropic effect of isoprenaline in rats
- Creator:
- Carusio, N., Wangensteen, R., Filippelli, A., and Ramaroson Andriantsitohaina
- Format:
- print, bez média, and svazek
- Type:
- article, články, model:article, and TEXT
- Subject:
- Experimentální medicína, fyziologie, polyfenoly, trombocyty, oxid dusnatý, physiology, polyphenols, thrombocytes, nitric oxide, Cognac, platelet aggregation, isoprenaline, 14, and 616-092
- Language:
- English
- Description:
- This study sought to evaluate whether consumption of polyphenol extract from Cognac (CPC) modulates platelet activation and cardiovascular reactivity in rats. Male Wistar rats were treated daily for 4 weeks by intra-gastric gavage receiving CPC at 80 mg/kg/day or vehicle (5 % glucose). Platelet adhesion and aggregation in response to different activators were assessed. Cardiac and vascular reactivity in response to various agonists as well as NO measurement by electron paramagnetic resonance technique were investigated in isolated heart and thoracic aorta. Oral administration of CPC decreased platelet aggregation induced by ADP but not by collagen. CPC did not affect adhesion to collagen. The chronotropic but not the inotropic response to isoprenaline was reduced without alteration of NO production in hearts from CPC-treated rats. CPC treatment did not affect ex vivo relaxation to acetylcholine nor NO content of rat aorta. CPC did not significantly alter the response to phenylephrine in aorta despite the participation of endothelial vasoconstrictor products. In summary, chronic treatment with CPC has no impact on ex vivo vascular and cardiac reactivity; however, it reduced heart work and platelet aggregation. These data suggest the existence of compounds in Cognac that may decrease the risk of coronary thrombosis and protect against some cardiac diseases., N. Carusio, R. Wangensteen, A. Filippelli, R. Andriantsitohaina., and Obsahuje bibliiografii a bibliografické odkazy
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
56. Oxidative stress and neuronal NOS activity: Putative determinants of rapid blood pressure increase after renal denervation in anesthetized rats
- Creator:
- Walkowska, A., Sadowski, J., and Kompanowska-Jezierska, E.
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, fyziologie člověka, human physiology, nitric oxide, renal denervation, free radicals, 14, and 612
- Language:
- English
- Description:
- Long-term effects of renal denervation (DNX) commonly include a decrease in blood pressure (BP), observed in both normotensive animals and various models of hypertension. On the other hand, short term BP re sponses vary. We examined how post-DNX increase in BP observed in this study depends on baseline metabolic and functional status of an imals, with a special interest for the role of oxidative stress. Anesthetized Wistar rats on standard (STD), low-sodium (LS) or high-sodium (HS) diet were used, untreated or pre-treated with tempol, a superoxide scavenger, or N(omeg a)-propyl-L-arginine (L-NPA), an inhibitor of neuronal NOS (nNOS). Early BP and renal hemodynamic responses were examined to right- and then left- side DNX performed using an own relatively non-invasive technique. Left kidney cortical, outer- and inner-medullary blood flows (CBF, OMBF, IMBF) were co ntinuously recorded as laser- Doppler fluxes. Sequential denervat ions significantly increased BP to final 19 %, 12 %, and 6 % above control level in HS, LS, and STD groups, respectively. CBF, a measure of total renal perfusion, increased in LS and STD but not in HS rats. Tempol pretreatment prevented the post-denervation BP increase on each diet. Selective inhibition of nNOS prevented BP increase in STD and HS groups, a modest incr ease persisted in LS rats. We propose that enhanced afferent impulsation from intrarenal chemoreceptors related to oxidative stress in the kidney was the background for acute BP increase after DNX. The response was triggered by a release of brain sympatho-excitatory centers from inhibition by renal afferents, this was followed by widespread sympathetic cardiovascular stimulation., A. Walkowska, J. Sadowski, E. Kompanowska-Jezierska., and Obsahuje seznam literatury
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
57. Participation of nitric oxide in different models of experimental hypertension
- Creator:
- Török, Jozef
- Format:
- print, bez média, and svazek
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, fyziologie, endotel, oxid dusnatý, endoteliální dysfunkce, hypertenze, physiology, endothelium, nitric oxide, endothelial dysfunction, hypertension, reactive oxygen species, arterial structural changes, NO-deficient hypertension, genetic hypertension, salt hypertension, 14, and 612
- Language:
- English
- Description:
- This review concerns the role of nitric oxide (NO) in the pathogenesis of different models of experimental hypertension (NO-deficient, genetic, salt-dependent), which are characterized by a wide range of etiology. Although the contribution of NO may vary between different models of hypertension, a unifying characteristic of these models is the presence of oxidative stress that participates in the maintenance of elevated arterial pressure and seems to be a common denominator underlying endothelial dysfunction in various forms of experimental hypertension. Besides the imbalance between the endothelial production of vasorelaxing and vasoconstricting compounds as well as the relative insufficiency of vasodilator systems to compensate augmented vasoconstrictor systems, there were found numerous structural and functional abnormalities in blood vessels and heart of hypertensive animals. The administration of antihypertensive drugs, antioxidants and NO donors is capable to attenuate blood pressure elevation and to improve morphological and functional changes of cardiovascular system in some but not all hypertensive models. The failure to correct spontaneous hypertension by NO donor administration reflects the fact that sympathetic overactivity plays a key role in this form of hypertension, while NO production in spontaneously hypertensive rats might be enhanced to compensate increased blood pressure. A special attention should be paid to the modulation of sympathetic nervous activity in central and peripheral nervous system. These results extend our knowledge on the control of the balance between NO and reactive oxygen species production and are likely to be a basis for the development of new approaches to the therapy of diseases associated with NO deficiency., J. Török., and Obsahuje bibliografii a bibliografické odkazy
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
58. Physical training limits the fall of blood pressure and the endothelium overactivation in acute myocardial infarction
- Creator:
- Manukhina, E. B., Lapshin, A. V., and Meerson, F. Z.
- Type:
- article, model:article, and TEXT
- Subject:
- nitric oxide, endothelium-dependent relaxation, exercise, adaptation, myocardial infarction, and hypotension
- Language:
- English
- Description:
- Physical training (PT) is beneficial in cardiovascular diseases associated with NO deficiency such as coronary disease, hypertension, etc. However, it is not known whether PT can also prevent pathological conditions associated with excess NO and fall of blood pressure (BP) such as acute myocardial infarction (AMI). The aim was to compare the effect of AMI on BP and functional state of the endothelium in rats trained by swimming and in untrained animals. After AMI, BP fell from 110±2 to 74±4 mm Hg (p<0.05), the endothelium-dependent relaxation increased from 37±4 to 66±6 % (p<0.05) and the extent of contraction suppression by the endothelium was significantly greater than in the controls. PT itself increased the endothelium-dependent relaxation of rat aorta but left BP unaffected. PT limited the AMI-induced fall of BP to 87±3 mm Hg, the endothelium- dependent relaxation to 53±4 % and prevented the hyporesponsiveness of the aorta to norepinephrine. We suggest that the protective effect of PT is related to inhibition of inducible NO synthase by a negative feedback mechanism.
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
59. Possible participation of EDRF-NO in the hormonal regulation of bone blood flow in rats
- Creator:
- Kapitola, J., Schreiber, V., Andrle, J., Haas, T., and Kubíčková, J.
- Type:
- article, model:article, and TEXT
- Subject:
- bone blood flow, endothelium-derived relaxing factor, nitric oxide, and rat
- Language:
- English
- Description:
- An increase in bone blood flow (BBF) was observed in rats after castration whereas a decrease in BBF occurred after oestradiol or testosterone. The possible participation of prostaglandins in these changes was demonstrated. The present results show that the endothelium-derived relaxing factor, i. e. nitric oxide (EDRF-NO), might play a role in these hormonal actions on BBF. Until now, almost nothing is known about the possible action of NO on bone circulation. Methylene blue (MB) as a substance blocking EDRF-NO was administered to sham-operated or oophorectomized (OOX) female rats. We determined local blood flow (85Sr-microsphere uptake), cardiac output, blood pressure, heart rate, density of the tibia and ash weight, as well as 24-h incorporation of 45Ca and 3H-proline into the tibia. The administration of MB (0.5 % in the food for 4 weeks) significantly lowered both 85Sr- microsphere uptake and blood flow values in the tibia and distal femur of sham-operated and OOX rats. MB lowered cardiac output and blood pressure to the same extent, indicating no change in the vascular resistance. After the administration of MB (0.1 % in the food), 85Sr-microsphere uptake decreased significantly in the tibia of OOX females while no significant change was found in soft tissues. Bone density and ash weight were significantly lower in OOX rats and in sham-operated rats after MB treatment. Finally, the 24-h incorporation of both 45Ca and 3H-proline decreased significantly in OOX females after MB administration (0.04 % in the food). It can be concluded that 1) MB lowers BBF, suggesting the participation of EDRF-NO in BBF regulation, 2) MB does not influence or may even suppress cardiac output and blood pressure in high dosage, 3) MB lowers 24-hour incorporation of 45Ca and 3H-proline into the tibia of OOX rats, which is in agreement with the circulatory effect, 4) MB lowers bone density and ash weight of the tibia in non-castrated female rats. The effects of MB observed in our experiments partially differ from those of arginine-derived blocking agents. This requires further elucidation.
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
60. Proceedings of the 6th International Symposium "Nitric Oxide: From Basic Regulations to Lifestyle-Related Disease": Tučepi (Croatia), September 16 - 21, 2009
- Format:
- Type:
- article, sborníky abstraktů, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, oxid dusnatý, mezinárodní konference, fyziologie, nitric oxide, international conferences, physiology, 14, and 612
- Language:
- English
- Description:
- Abstrakty příspěvků z konference
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public