The development of pulmonary hypertension involves a complex process. Some patients have “unknown” causes, some are hereditary, and some have specific etiologies. Overall, however, the specific mechanisms that trigger pulmonary hypertension are not well understood. It is generally believed that pulmonary hypertension may be caused when an abnormal process occurs in the inner layer of the pulmonary artery. The inner layer of pulmonary hypertension is composed of endothelial cells that secrete many chemicals that keep the blood vessels functioning properly. When you have pulmonary hypertension, the balance between these chemicals is lost. Levels of endothelin and thromboxane increase and levels of prostacyclin and nitric oxide decrease, resulting in abnormal pulmonary artery function: 1. abnormal contraction and diastole of the blood vessels; 2. uncontrollable cell growth; 3. the cells that control the contraction and diastole of the blood vessels (smooth muscle cells) become large and covered with scar tissue (due to “fibrosis”) and cannot 4. senescent cells that should have died and been removed continue to live and remain in the blood vessels, increasing the amount of cells in each lining; 5. blood cells, such as platelets and red blood cells, along with excess fibrous material, bind to each other in the blood vessels, forming large clots called “thrombi”.