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Journal Biomedical Radioelectronics №5 for 2016 г.
Article in number:
Noradrenaline-evoked restoration of the neurogenic vasoreactivity diminished by nitric oxide
Authors:
V.N. Yartsev - Ph.D. (Biol.), Senior Research Scientist, Pavlov Institute of Physiology, Russian Acad. Sci., Saint-Petersburg, Russia. E-mail: yartsev@infran.ru
Abstract:
Neurogenic tone of the blood vessels, which can be regarded as one of the most impotent means of the central regulation of the circulation, depends significantly on the hormones and other factors of the local control of blood flow [1]. We have previously shown for the first time that noradrenaline (NA) is able to restore neurogenic contraction of the isolated segments of the rat tail artery diminished by acidosis [2]. Since acidosis-induced vasodilatation at least in part results from the effect of endothelium-derived nitric oxide (NO) [3], we hypothesized that NA might restore neurogenic vasoconstriction diminished by NO. The aim of this work was to check our hypothesis. The experiments were carried out on the isolated segments of the rat tail artery. Neurogenic contraction of the vessel segment was evoked by periodic electrical field stimulation (EFS) (conducted at a frequency of 3, 10, and 40 Hz every 3 min) of perivascular nerves in the vessel segment before and after addition of NA in cumulative concentration (from 0.03 μM to 10 μM). One of the two series of experiments served as a control while in the second series, sodium nitroprusside (10 μM) used as NO donor was applied 30 min before addition of NA. NO was shown to decrease considerably the artery reaction to NA and EFS which was not the case at high frequency of EFS (10-40 Hz) delivered at high NA concentration (0.5-1.0 μM). In the presence of NO, NA-evoked potentiation of the neurogenic tone produced by 3 Hz EFS at low NA concentration (0.03-0.1 μM) was smaller than in control, while at 10-40 Hz it was equal to that in the control. NA-evoked potentiation of the neurogenic tone produced by 3 Hz EFS at high NA concentration (0.5-1.0 μM) was almost equal to that in the control, while at 10-40 Hz it was significantly larger than in control. In the presence of NO, NA-evoked potentiation of the neurogenic tone produced by high frequency EFS (10-40 Hz) was significantly larger than produced by 3 Hz EFS, while in control the potentiation was almost the same at all frequencies. Change in the profile and degree of the NA-evoked potentiation of the neurogenic vasoconstriction produced by EFS at frequencies of 3-40 Hz in the presence of NO was identical to that for acidosis. We believe that the increased NA-evoked potentiation of the neurogenic constriction of the rat tail artery shown in our experiments in the presence of NO at higher EFS frequencies and NA concentrations may be of importance for the blood flow redistribution in favor of vital organs at strenuous exercise which is known to be accompanied by increased acidosis-dependent and/or acidosis-independent NO production, high-frequency sympathetic nerve activity, and high level of NA.
Pages: 66-68
References

 

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