Smoking causes hypoxic vasospasm, thickening, and inflammation. Such responses are similar to the pathological mechanism of pulmonary arterial hypertension (PAH). PAH is a progressive and fatal disease that is characterized by the irreversible remodeling of the pulmonary artery. Pulmonary vasospasm, thickening, and inflammation are triggered by a chronic increase in cytosolic Ca 2+ concentration. Here, we focused on the expression of nicotinic acetylcholine receptors (nAChRs), which are associated with cytosolic Ca 2+ signaling, in PAH and hypoxic stress. The expression of the α subunits of nAChRs in pulmonary arterial smooth muscle cells (PASMCs) from normal subjects and idiopathic pulmonary arterial hypertension (IPAH) patients was analyzed by RT-PCR. Normal-PASMCs expressed nAChRα5 and α9 subunits. On the other hand, IPAH-PASMCs expressed nAChRα1, α5, and α7 subunits. As a result of Western blotting, the expression of nAChRα1and α7 proteins was upregulated in IPAH-PASMCs. In addition, the expression of nAChRα1 subunits was also increased in PASMCs from monocrotalineinduced pulmonary hypertensive rats. Furthermore, hypoxic exposure (1% O 2 ) increased nAChRα7 expression in normal-PASMCs. In conclusion, the expression of nAChRα1 and α7 subunits is upregulated in chronic respiratory diseases including PAH and hypoxic stress.