Journal of Applied Physiology, Vol 76, Issue 2 916-922, Copyright © 1994 by American Physiological Society
Endogenous vasodilators modulate pulmonary vascular anaphylaxis
L. J. Kelly, B. J. Undem and G. K. Adams 3rd
Johns Hopkins University School of Medicine, Baltimore, Maryland 21224.
We examined the role of endothelium-derived nitric oxide during
antigen-induced contraction in pulmonary arteries isolated from actively
sensitized guinea pigs. Ovalbumin (10(-2) mg/ml)-induced contraction was
not sustained, and tension returned to baseline within 15 min. Pretreatment
with methylene blue (10(-5) M) increased both the amplitude and the
duration of the contractile response in these tissues. At 15 min, tension
remained elevated and was > 70% of the peak amplitude. Removal of the
endothelium with saponin (200 micrograms/ml) increased the magnitude of the
contraction by > 125%; however, the duration of the response was
unaffected. After pretreatment with saponin, methylene blue no longer
increased the amplitude of antigen-induced contraction but its effect on
the duration was unchanged. Pretreatment with nitro-L-arginine methyl ester
significantly increased the magnitude of the contraction in each of the
tissues. These results suggest that the response of guinea pig pulmonary
arteries to antigen is modulated by two types of endogenous vasodilators,
endothelium-derived nitric oxide that inhibits the initial phase of the
response and an endothelium-independent relaxing factor that is guanosine
3',5'-cyclic monophosphate dependent and attenuates the duration of
anaphylactic contraction.
