Nitrate- Nitrite- Nitric Oxide Pathway in Pulmonary Arterial Hypertension Therapeutics
Pulmonary arterial hypertension (PAH) is a disorder characterized by elevated vascular resistance in pulmonary arterioles. Progressive increases in pulmonary vascular resistance and pulmonary artery pressures result in right heart failure and reduced cardiac output. Patients experience progressive exertional dyspnea, right heart failure, syncope, and ultimately death. The common pathophysiological features of PAH include pulmonary vasoconstriction, intimal and smooth muscle proliferation, in situ thrombosis, and pathological remodeling of pulmonary arterial circulation. While the origin of PAH is multifactorial, impairments in vasodilator (nitric oxide and prostaglandin signaling) and vasoconstrictor (endothelin-1, reactive oxygen species, angiotensin II) pathways underlie the evolution of early disease.1 Based on this knowledge, drugs that enhance the NO signaling pathways (phosphodiesterase 5 inhibitors), the prostenoids, and endothelin receptor blockers, have been developed and approved for PAH specific therapy. (SELECT FULL TEXT TO CONTINUE)
- Received April 18, 2012.
- Accepted April 19, 2012.
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