NG-Nitro-L-arginine Methyl Ester-Induced Potentiaton of the Effect of Aminophylline on Rat Diaphragm: the Role of Extracellular Calcium

Stojanović, Rastko; Todorović, Zoran; Nesic, Zorica; Vučković, Sonja; Cerovac-Cosic, Natasa; Prostran, Milica

doi:10.1254/jphs.sce04001x

Cited by 15 publications

(19 citation statements)

References 16 publications

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“…The present experiments with nicardipine confirm that diaphragm is a specific skeletal muscle whose contraction is more dependent on external calcium than other skeletal muscles (2,10,11,15). More profound, dose-related depression of Nor effects on Td in the presence of micromolar nicardipine during DSTES might indicate a use-dependent block of sarcolemal voltage calcium channels (i.e., channels that are being used frequently are more susceptible to block).…”

supporting

confidence: 62%

“…Both signals could be modulated with dihydropyridine-receptor agonists and antagonists (9). The isometric contraction of the rat diaphragm is dependent on external calcium, contrary to the other types of skeletal muscle (10,11).…”

mentioning

confidence: 99%

“…The investigation conforms to the Guide for the Care , Galenika, Serbia and Montenebro). The doses of the drugs used were selected according to the receptor affinities (7), our published data (e.g., 1,10,14), as well as preliminary dose-finding studies. Results are expressed as the mean ± S.E.M.…”

mentioning

confidence: 99%

“…Besides enhanced depletion of SR calcium stores during repetitive, high frequency stimulation by cumulative Nor (DSTES), sarcolemal L-calcium channels seem to enter more readily the inactive state in such conditions (dihydropyridines possess higher affinity for inactivated calcium channels). On the other hand, the nitric oxide (NO)-induced depression of Td in such a model could be rejected because NO synthase in the diaphragm is a calcium-dependent isoform (10). However, in the presence of nicardipine, Nor seems to be able to trigger another NO-unrelated cascade in the diaphragm that could produce membrane hyperpolarization (e.g., increase in intracellular protein kinase A and modulation of sarcolemal potassium channels); further, more detailed investigation is necessary to clarify such a mechanism.…”

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confidence: 99%

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Type of Electrical Stimulation Influences Diaphragm Response to Adrenoceptor and Calcium Channel Modulators: the Role of Extracellular and Intracellular Calcium Events

et al. 2006

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Abstract. The influence of direct single pulse and subtetanic electrical stimulation (ES) on isolated rat hemidiaphragm response to adrenoceptor antagonists and calcium channel blockers was investigated. Muscle contractility was stimulated by cumulative micromolar noradrenaline. Noradrenaline effects on developed tension (Td) in the presence of various α-and β-adrenoceptor antagonists (e.g., prazosin and ICI 118551) were qualitatively different during different types of ES. Also, intact L-voltage calcium channels were necessary for noradrenaline-induced potentiation of Td during both types of ES, while the balance between ryanodine receptors-and inositol triphosphate (IP 3 )-related calcium events in the muscle was influenced by the pattern of the ES.

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confidence: 62%

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confidence: 99%

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confidence: 99%

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Type of Electrical Stimulation Influences Diaphragm Response to Adrenoceptor and Calcium Channel Modulators: the Role of Extracellular and Intracellular Calcium Events

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“…In a calcium-free medium, L-NAME completely abolished the effect of AMPh on diaphragm contractility. The finding that L-voltage Ca 2+ chanel blockers (verapamil and nicardipine) did not significantly change the L-NAME-induced potentiation of the stimulatory effect of AMPh suggests that the influx of extracellular calcium through L-voltage Ca 2+ channels of sarcolema is not necessary for such an interaction between L-NAME and AMPh (9,10). Therefore, it was of interest to assess whether such an interaction could be modulated by the different frequencies of the DSES.…”

Section: G -Nitro-l-arginine Methyl Ester Stimulation Frequencymentioning

confidence: 99%

Aminophylline Pretreatment Modulates the Nitric Oxide System of the Isolated Rat Diaphragm: the Role of Frequency of the Electrical Stimulation

et al. 2005

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Abstract. The effect of different frequencies of direct subtetanic electrical stimulation (14, 20, and 30 Hz) and aminophylline (AMPh) pretreatment on the effect of N G -nitro-L-arginine methyl ester (L-NAME) (1 mM) on isolated rat diaphragm was investigated. L-NAME potentiated tension developed (Td) in the diaphragm pretreated with a single concentration of AMPh (1.08 mM) in a frequency-dependent manner. The effect was significantly different in comparison with muscle incubated 30 min with Tyrode solution only. In the muscle pretreated with cumulative concentrations of AMPh (0.36 -3.60 mM), the frequency-dependent potentiation of Td induced by L-NAME and the difference between L-NAME-treated and untreated muscle were lost.After the discovery of the nitric oxide (NO) system in skeletal muscle, the influence of NO and inhibitors of NO synthase (NOS) on muscle contractility were investigated (1, 2). Kobzik et al.(1) have shown that blockade of NOS in the isolated rat diaphragm produced an increase of muscle contractility. They postulated that inhibitors of NO (i.e., 7-nitroindazole, aminoguanidine, and nitro-L-arginine) have a specific, NO-related effect on the muscle contractility. However, some authors observed NO-unrelated effects of NOS inhibitors (3).NO is synthesized continually at low rates by constitutive isoforms of NOS, the synthesis of NO being increased during repetitive isometric contractions up to 200% (4). NO may modulate skeletal muscle contractility via at least two mechanisms, through the cGMP-NO pathway, and directly, by interacting with calcium release channels of the sarcoplasmic reticulum (5). The effects of NO on the channel activity primarily depend on its concentration, and its interaction with reactive oxygen species (ROS) (2). Reid et al. (6) have shown that superoxide generated by diaphragm muscle bundles increases both twitch and tetanic forces developed, a deesterifed form of L-NAME, in the concentration range used in our experiments (≥1 mM) blocked NOS activity in the skeletal muscle (e.g., rat diaphragm, extensor digitorum longus) (1,7,8).The diaphragm is the primary muscle of inspiration. The relationship between the diaphragm contractile function and NO-synthase activity could have therapeutic significance in neuromuscular diseases associated with changes in muscle fibers and activity of the NO system. Consequently, the effects of various NOS inhibitors on diaphragm contractility have been evaluated during the last decade (1, 2).The interaction between L-NAME and aminophylline (AMPh) on the contractility of the isolated rat diaphragm stimulated by direct subtetanic electrical stimulation (DSES) and the role of extracellular calcium in such an interaction were already investigated. It was shown that the stimulatory effects of cumulative concentrations of AMPh on the contractility of the isolated rat diaphragm during DSES (14 Hz) were potentiated by L-NAME. In a calcium-free medium, L-NAME completely abolished the effect of AMPh on diaphragm

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A selective beta2-adrenergic agonist, terbutaline, improves sepsis-induced diaphragmatic dysfunction in the rat

et al. 2006

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NG-Nitro-L-arginine Methyl Ester-Induced Potentiaton of the Effect of Aminophylline on Rat Diaphragm: the Role of Extracellular Calcium

Cited by 15 publications

References 16 publications

Type of Electrical Stimulation Influences Diaphragm Response to Adrenoceptor and Calcium Channel Modulators: the Role of Extracellular and Intracellular Calcium Events

Type of Electrical Stimulation Influences Diaphragm Response to Adrenoceptor and Calcium Channel Modulators: the Role of Extracellular and Intracellular Calcium Events

Aminophylline Pretreatment Modulates the Nitric Oxide System of the Isolated Rat Diaphragm: the Role of Frequency of the Electrical Stimulation

A selective beta2-adrenergic agonist, terbutaline, improves sepsis-induced diaphragmatic dysfunction in the rat

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