To determine whether nitric oxide (NO) contributes to the hypotensive state induced by exposure to radiofrequency radiation of millimeter-wavelength. To explore this question, a synthetic analogue of L-arginine, Nw-nitro-L-arginine methyl ester (L-NAME), was used to pharmacologically inhibit the synthesis of NO following millimeter wavelength exposure.
(NO is a potent endogenous vasodilator produced from the guanidino nitrogen group of L-arginine by the enzyme nitric oxide synthase (NOS). Under physiological conditions, the release of NO by NOS in vascular endothelial cells dilates blood vessels and, in concert with vasoconstrictor catecholamines, regulates blood vessel diameter, organ blood flow, and blood pressure. Pathological increases in NO release have been shown to mediate hypotensive states and circulatory shock.)
|Distance between exposed object and exposure source||1.1 m|
|Exposure room||RF-shielded anechoic chamber (27°C, 20% humidity), holder consisting of seven 0.5cm Plexiglas rods mounted in a semicircular pattern on 4 cm x 6 cm Plexiglas plates (0.5 cm thick)|
|Setup||The animal was centered along the boresight and exposed in an E-orientation|
Acute pharmacological blockade of NO synthesis following the induction of cardiovascular failure by millimeter wavelength exposure does not ameliorate the hypotensive state and is not of survival benefit to the animal, suggesting that excess levels of NO do not mediate this form of circulatory failure.