Endogenous vasodilators modulate pulmonary vascular anaphylaxis. J. Ap
pl. Physiol. 76(2): 916-922, 1994. - We examined the role of endotheli
um-derived nitric oxide during antigen-induced contraction in pulmonar
y arteries isolated from actively sensitized guinea pigs. Ovalbumin (1
0(-2) mg/ml)-induced contraction was not sustained, and tension return
ed to baseline within 15 min. Pretreatment with methylene blue (10(-5)
M) increased both the amplitude and the duration of the contractile r
esponse in these tissues. At 15 min, tension remained elevated and was
>70% of the peak amplitude. Removal of the endothelium with saponin (
200 mu g/ml) increased the magnitude of the contraction by >125%; howe
ver, the duration of the response was unaffected. After pretreatment w
ith saponin, methylene blue no longer increased the amplitude of antig
en-induced contraction but its effect on the duration was unchanged. P
retreatment with nitro-L-arginine methyl ester significantly increased
the magnitude of the contraction in each of the tissues. These result
s suggest that the response of guinea pig pulmonary arteries to antige
n is modulated by two types of endogenous vasodilators, endothelium-de
rived nitric oxide that inhibits the initial phase of the response and
an endothelium-independent relaxing factor that is guanosine 3', 5'cy
clic monophosphate dependent and attenuates the duration of anaphylact
ic contraction.