Estrogens have remarkable roles in various diseases and physiological events. The recent studies indicate that estrogens exhibit rapid effects such as calcium influx or release of nitric oxide via receptors on the cell membrane or on endoplasmic reticulum. This receptor is called GPER-1 (G protein-coupled estrogen receptor-1). In many previous studies, acute administration of GPER-1 selective agonist G1 reduced ischemia/reperfusion (I/R) injury in heart. In this study, the effect of G1 on the pulmonary vascular bed was investigated using isolated organ bath and isolated lung perfusion. The effect of pre-ischemic acute G1 treatment on lung I/R injury was assessed with post-I/R acetylcholine (ACh) or sodium nitroprusside (SNP) administration. Lungs wet/dry weight ratios were measured to determine the role of acute G1 administration on lung edema due to I/R injury. G1 was not cause a vasorelaxation in precontracted pulmonary arteries. The acute G1 pre-administration was increased the responses of ACh and SNP in I/R injury, however this increase was not statistically significant compared to control. There was no change on lung wet/dry weight ratio between the treatment and control groups. The vasorelaxation responses to ACh and SNP were not different between male and female rats. In our study, G1 caused a slight vasorelaxation in pulmonary vascular bed. There was no significant increase in the vasorelaxations with G1 treatment after I/R injury. Our results suggest that considering the presence of GPER-1 in lung tissue, GPER-1 should be evaluated in detail with further studies.