Abstract
Pulmonary hypertension (PH) is a severe disease affecting both the pulmonary and systemic circulation. One of possible factors of these disturbances can be nitric oxide (NO) overproduction by inducible NO synthase (iNOS). To examine the effect of iNOS on systemic vascular reactivity, we used aminoguanidine (AG), a selective iNOS inhibitor. Using the model of monocrotaline-induced pulmonary hypertension, we demonstrated that chronic AG administration restores the decreased arterial pressure responses to NO donor and to nonspecific inhibitor of NO synthase as well as the decreased endothelium-dependent relaxation of isolated systemic artery. This points to an important role of iNOS in systemic pathogenesis of PH.
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