Obstructive sleep apnea, a breathing disorder featured by chronic intermittent hypoxia (CIH) is associated with moderate pulmonary hypertension (PH), but the underlaying mechanisms are not well-known. STIM-activated Ca2+ TRPC-ORAI channels (STOC) are overexpressed in the lung and play a key role in the development of lung vascular remodeling and PH in animals exposed to sustained hypoxia. However, whether these channels are involved in the lung vascular remodeling and PH induced by CIH has not been studied. Thus, we assessed the effects of 2-aminoethyldiphenylbonirate (2-APB), a STOC blocker on lung vascular remodeling and PH in rats exposed to CIH. Male Sprague-Dawley rats (∼200g) were exposed to CIH (5% O2, 12 times/h for 8h). At 14 days of CIH, rats under isoflurane anesthesia were implanted with osmotic pumps containing 2-APB (10mg/kg(day) or its vehicle, and then were exposed to CIH for 14 more days. At the end of CIH exposure, the right ventricular systolic pressure (RVSP) was measure, and the lungs were dissected to determine the remodelling and mRNA levels of STOC subunits TRPC1, TRPC4, TRPC6, ORAI1 and ORAI2 by qPCR. 2-APB prevented the increase in RVSP (35.5 ± 1.1 mmHg vs. 24.7 ±1.6 mmHg, p< 0.05, CIH vs. CIH-2-APB, respectively), and the increase of the media tickness in pulmonary arteries of 200 µm (66.3 ± 9.4% vs. 48.2 ± 3.5%, p<0.05, CIH vs. CIH-2APB, respectively). In addition, 2-APB treatment reverted the increase in the mRNA levels of TRPC1, TRPC4 and TRPC6, but induced an overexpression of ORA1, while ORAI2 remainned unchanged. Present results suggest that STOC plays a crucial role in the develop of the vascular remodeling and PH induced by CIH.