Active vasodilation during fainting: A hypothesis revisited

The current concept is that the vasodilation which contributes to fainting (vasovagal syncope) is caused entirely by withdrawal of sympathetic vasoconstrictor tone (i.e. passive vasodilation).(1,2) This concept has supplanted the idea that an active, sympathetically mediated component to the vasodilation exists in humans.(3) We have several lines of evidence suggesting that there can be sympathetically mediated active vasodilation in humans. We speculate that this active vasodilation may be linked to the release of the recently identified vasodilator nitric oxide. Along these lines, we have experimental evidence consistent with neurally mediated nitric oxide release during several types of sympathoexcitatory maneuvers in humans. We have also observed forearm vasodilation during a vasovagal response after alpha-adrenergic blockade of the forearm under study. These observations indicate that the potential role of active vasodilation during fainting in humans should be revisited.