The present invention is based upon the observation that inhibition of NPR-CSignaling pathway leads to the development of pulmonary arterial hypertension(PAH). Accordingly, the invention provides a mouse model for PAH, andproposes a method of using synthetic analogs of the NPR-C signaling pathway,specifically synthetic C-type atrial natriuretic factor or intermediates for,ormodulators of, the NPR-C signaling pathway as anti-pulmonary vasculopathyagents. Activators of the NPR-C signaling pathway are disclosed to treat orprevent vasculopathy, including but not limited to PAH and other types ofpulmonary hypertension, peripheral vascular disease, critical limb ischemia,coronary artery disease, and diabetic vasculopathy.
