Production and Storage of Nitric Oxide in Adaptation to Hypoxia

Манухина, Е. Б.; Malyshev, I. Yu.; Smirin, Boris V.; Mashina, S. Yu.; Saltykova, V. A.; Vanin, Anatoly F.

doi:10.1006/niox.1999.0244

Cited by 47 publications

(36 citation statements)

References 20 publications

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“…Thus, NO levels will be reported as NO X . In mammals, this method demonstrates high accuracy and reproducibility and adequately reflects actual NO production (Gilliam et al, 1993;Manukhina et al, 1999). It is possible that NO levels could be underestimated, however, owing to the exit of nitrite (formed from NO) from the plasma or perfusate through Cl -channels; this potential underestimation, however, would be expected to be constant among the treatment groups.…”

Section: No Assaymentioning

confidence: 99%

The interactive effects of hypoxia and nitric oxide on catecholamine secretion in rainbow trout (Oncorhynchus mykiss)

McNeill

Perry

2006

Journal of Experimental Biology

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SUMMARY Experiments were performed to test the hypothesis that exposure of rainbow trout to repetitive hypoxia would result in a decreased capacity of chromaffin cells to secrete catecholamines owing to increased production of nitric oxide(NO), a potent inhibitor of catecholamine secretion. A partial sequence of trout neuronal nitric oxide synthase (nNOS) was cloned and its mRNA was found to be present in the posterior cardinal vein (PCV), the predominant site of chromaffin cells in trout. Using heterologous antibodies, nNOS and endothelial NOS (eNOS) were localized in close proximity to the chromaffin cells of the PCV. Exposure of trout to acute hypoxia (5.33 kPa for 30 min) in vivoresulted in significant increases in plasma catecholamine and NO levels. However, after 4 days of twice-daily exposures to hypoxia, the elevation of plasma catecholamine levels during hypoxia was markedly reduced. Associated with the reduction in plasma catecholamine levels during acute hypoxia was a marked increase in basal and hypoxia-evoked circulating levels of NO that became apparent after 2-4 days of repetitive hypoxia. The capacity of the chromaffin cells of the hypoxia-exposed fish to secrete catecholamine was assessed by electrical stimulation of an in situ saline-perfused PCV preparation. Compared with control (normoxic) fish, the PCV preparations derived from fish exposed to repeated hypoxia displayed a significant reduction in electrically evoked catecholamine secretion that was concomitant with a marked increased in NO production. This additional rise in NO secretion in preparations derived from hypoxic fish was prevented after adding NOS inhibitors to the perfusate; concomitantly, the reduction in catecholamine secretion was prevented. The increased production of NO during hypoxia in vivo and during electrical stimulation in situ was consistent with significant elevations of nNOS mRNA and protein; eNOS protein was unaffected. These results suggest that the reduced capacity of trout chromaffin cells to secrete catecholamines after repeated hypoxia reflects an increase in the expression of nNOS and a subsequent increase in NO production during chromaffin-cell activation.

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Section: No Assaymentioning

confidence: 99%

The interactive effects of hypoxia and nitric oxide on catecholamine secretion in rainbow trout (Oncorhynchus mykiss)

McNeill

Perry

2006

Journal of Experimental Biology

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“…Therefore, NO production was evaluated indirectly by measuring the concentration of nitrite and nitrate, stable metabolites of NO in biological fluids. This method demonstrates high accuracy and reproducibility and adequately reflects actual NO production (Gilliam et al, 1993;Manukhina et al, 1999). The NO assay was performed as described by Gilliam et al (1994), with modifications.…”

Section: Nitric Oxide Assaymentioning

confidence: 99%

Nitric oxide and the control of catecholamine secretion in rainbow trout Oncorhynchus mykiss

McNeill

Perry

2005

Journal of Experimental Biology

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SUMMARY An in situ saline-perfused posterior cardinal vein preparation was used to assess the role of nitric oxide (NO) in the regulation of basal and stimulus-evoked catecholamine secretion from rainbow trout Oncorhynchus mykiss chromaffin cells. Addition of the NO donor, sodium nitroprusside(SNP) to the inflowing perfusate abolished catecholamine secretion during electrical field stimulation, thereby establishing the potential for NO to act as a potent inhibitor of catecholamine release. A possible role for endogenously produced NO was established by demonstrating that stimulus-evoked(depolarizing levels of KCl or electrical field stimulation) catecholamine secretion was markedly stimulated in the presence of the nitric oxide synthase(NOS) inhibitors l-NAME and 7-NI. Although in vitroexperiments demonstrated that catecholamine degradation was enhanced by NO in a dose-dependent manner, the dominant factor contributing to the reduction in catecholamine appearance in the perfusate was specific inhibition of catecholamine secretion. Subsequent experiments were performed to identify the NOS isoform(s) contributing to the inhibition of stimulus-evoked catecholamine secretion. Inducible NOS (iNOS; an enzyme that can be activated in the absence of Ca2+), although present in the vicinity of the chromaffin cells(based on mRNA measurements), does not appear to play a role because stimulus-evoked NO production was eliminated during perfusion with Ca2+-free saline. The potential involvement of endothelial NOS(eNOS) was revealed by showing that hypoxic perfusate evoked NO production and corresponded with an inhibition of stimulus-evoked catecholamine secretion;chemical removal of the endothelium (using saponin) prevented the production of NO during hypoxia. However, because removal of the endothelium did not affect NO production during electrical field stimulation, it would appear that the neuronal form of NOS (nNOS) is the key isoform modulating catecholamine secretion from trout chromaffin cells.

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“…With the use of EPR spectroscopy, it has been found that the NO production increased after 5 minutes of ischaemia and continued for 60min . The NO overproduction in acute hypoxia has also been noted (Manukhina et al 1999). In a number of studies with some models of cerebral ischaemia, results were obtained which do not coincide with the point of view of the neurotoxic role of ischaemia generated NO.…”

Section: Discussion Of the Results Of Experimentsmentioning

confidence: 99%

Participation of NO-synthase in Control of Nitric Oxide Level in Rat Hippocampus after Modelling of Ischaemic and Haemorrhagic Insult

Гайнутдинов¹,

Pashkevich²,

Андрианов³

et al. 2017

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Electron paramagnetic resonance (EPR) was used as a method for recording the content of the nitric oxide (NO) in hippocampal tissues of intact rats and rats after modelling of ischaemic and haemorrhagic stroke. Based on direct measurements of NO by EPR spectroscopy, it was shown that, within 5 hours after the onset of symptoms of ischaemic and haemorrhagic stroke, the formation of NO in the hippocampus was reduced by a factor of 2-3 and this reduction was maintained for a period of between 24 and 72 hours. The results show that a systemic character of a decrease in the intensity of NO production during the modelling of ischaemic events in the brain reflects the effects of central dysregulation of the functions at the level of the whole organism such that it is appropriate to consider implementing the correction of the vital systems of the body in a stroke. It has indicated that non-selective NO-synthase blocker L-NAME reduced the low level of NO production by a factor of 3 by its administration within 72 hours after post-ischaemic and haemorrhagic stroke. It was discovered however that L-NAME returns the level of NO production to baseline (control) by its administration within 5 hours after ischaemia.

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Production and Storage of Nitric Oxide in Adaptation to Hypoxia

Cited by 47 publications

References 20 publications

The interactive effects of hypoxia and nitric oxide on catecholamine secretion in rainbow trout (Oncorhynchus mykiss)

The interactive effects of hypoxia and nitric oxide on catecholamine secretion in rainbow trout (Oncorhynchus mykiss)

Nitric oxide and the control of catecholamine secretion in rainbow trout Oncorhynchus mykiss

Participation of NO-synthase in Control of Nitric Oxide Level in Rat Hippocampus after Modelling of Ischaemic and Haemorrhagic Insult

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