Does nitric oxide attenuate platelet-activating factor induced nasal airway plasma extravasation in healthy subjects?
Topical administration of a NO inhibitor is able to attenuate the nasal airway plasma extravasation induced by PAF, suggesting that NO release in vivo is involved in the nasal response to PAF.
A direct effect of D2O on [Ca2+]i in vascular endothelial cells may be responsible for the endothelium-dependent, presumably nitric oxide-mediated, vasodilation induced by D2O in precontracted vessels. From these results new mechanisms can be explored for the antihypertensive effect of D2O and new avenues can be developed to study the functional integrity of the endothelium-dependent regulation of the vascular tone.