The present study demonstrated that 1) chronic IH increases pro-inflammatory macrophages with upregulation of β3AR and iNOS in the lungs, 2) IH-derived activation of β3AR/iNOS signaling promotes NO secretion from pulmonary macrophages, and 3) that the pulmonary macrophages attenuate HPV via the β3AR/iNOS signaling pathway in IH rats. The gene discussed is ADRB3; the disease is isolated hemihyperplasia.