Vasodilation induced by PPARβ /δ agonists is greater at higher pressures than lower pressures in rat pulmonary arteries

Pulmonary arterial hypertension (PAH) is defined as a mean pulmonary artery pressure of greater than 25mmHg at rest, and advanced PAH as 50-60mmHg. Current therapies include prostacyclin (IP) receptor agonists (e.g. iloprost and beraprost), phosphodiesterate type 5 inhibitors (e.g. sildenafil), and endothelin receptor antagonists (e.g. bosentan). However, none of these drugs cure the condition, and new therapeutic approaches are currently under investigation. We and others have recently shown that the PPARβ/δ agonist GW0742 induces vasodilatation of mouse and rat pulmonary arteries (Harrington et al 2010; Li et al 2012). However, the effects of pressure on the vasodilatory effects of PPARβ/δ agonists have not been tested. Here we investigated vasodilation induced by PPARβ/δ agonists in rat pulmonary arteries at different resting pressures in line with those seen in patients with PAH