The purpose of this in vitro study was to determine whether radiofrequency burst-type electromagnetic fields may facilitate NO synthesis, activate guanylate cyclase and increase the production of cyclic GMP.
Rat cerebellum supernatant was used. Recently, it has been established, that guanylate cyclase is activated by a catalytic action of NO synthase (NO synthase is prominently localized in the cerebellum tissues).
In an in vivo study (using the arterioles of the frog web) the relation of NO synthesis with the vasodilatory effect was studied.
|Duty cycle||50 %|
|Repetition frequency||10 kHz|
|Duty cycle||100 %|
|cf. remarks||-||-||-||-||U = 5 V peak-to-peak|
When the supernatant was incubated with both exogenous L-arginine (NO donor) and NADPH, and irradiated by an radiofrequency burst-type electromagnetic field, the production of cyclic GMP was increased significantly. By contrast, such an effect was not found when the cerebellum supernatant was irradiated by an radiofrequency field volley-type electromagnetic field.
When neither L-arginine nor NADPH were added to the supernatant, the production of cyclic GMP was lowered and the exposure effect was not found.
Incubation with Methylene Blue, a guanylate cyclase inhibitor, lowered the production of cyclic GMP and the exposure effect did not occur. On incubation with a NO synthase inhibitor, the production of cyclic GMP was lowered and the irradiation effect was not observed.
Using electrochemical NO probes, the production of NO in the supernatant was detected. The concentration of NO increased after the onset of the electromagnetic field exposure. The irradiation effect persisted, and reached a maximum after the cessation of the exposure.
The arterioles of the frog web were dilated by the exposure, and this effect was almost completely abolished by the addition of a NO synthase inhibitor. This indicates that exposure activates NO synthase and induces vasodilatation.