Quiescent pulmonary endothelium establishes an anti-thrombotic, anti-inflammatory surface that promotes blood flow. However, the endothelium rapidly responds to injury and inflammation by promoting thrombosis and enabling the directed transmigration of inflammatory cells, such as neutrophils, into the alveolar airspace. While the endothelial cell signals responsible for establishing a pro-thrombotic surface are distinct from those responsible for recognizing circulating neutrophils, these processes are highly inter-related. Von Willebrand factor stimulated secretion plays an important role in thrombus formation, while P-selectin surface expression plays a key role in neutrophil binding necessary for transmigration. Both von Willebrand factor and Pselectin are located within Weibel-Palade bodies in pulmonary arteries and arterioles, yet WeibelPalade bodies are absent in capillaries. Despite the absence of the Weibel-Palade bodies, pulmonary capillaries express both von Willebrand factor and P-selectin. The physiological and pathophysiological significance of these observations is unclear. In this review, we address some anatomic and physiologic features that distinguish pulmonary artery, capillary, and vein endothelium. In addition, we review our current understanding regarding the stimulated secretion of von Willebrand factor and P-selectin in pulmonary artery and capillary endothelium. This information is considered in the context of vasculitis and pneumonia, two pathophysiological processes to which the stimulated secretion of von Willebrand factor and P-selectin contribute.