title: Shear stress-mediated F1/FO ATP synthase-dependent CO2 gas excretion from human pulmonary arteriolar endothelial cells.
abstract: We studied the physiological role of flow through pulmonary arterioles in CO(2) gas exchange. We established human pulmonary arteriolar endothelial cells (HPAoEC). The cells demonstrated marked immunocytochemical staining of PECAM-1, VEGF R2, ACE-1, and CA type IV on their cell surface. Ten seconds shear stress stimulation caused the co-release of H(+) and ATP via the activation of F(1)/F(O) ATP synthase on the HPAoEC. F(1)/F(O) ATP synthase was immunocytochemically observed on the cell surface of non-permeabilized HPAoEC. In the shear stress-loaded HPAoEC culture media supernatant, ATPase activity increased in a time-dependent manner. The HPAoEC were strongly stained for NTPDase 1, which partially co-localized with purinergic P2Y1. The purinergic P2Y1 receptor agonist UTP (10(-6) M) significantly potentiated the shear stress-induced increase in ATPase activity in the culture medium supernatant. Ten seconds shear stress stimulation also produced stress strength-dependent CO(2) gas excretion from the HPAoEC, which was significantly reduced by the inhibition of F(1)/F(O) ATP synthase or CA IV on the endothelial cell (EC) surface. In conclusion, we have proposed a new concept of CO(2) exchange in the human lung, flow-mediated F(1)/F(O) ATP synthase-dependent H(+) secretion, resulting in the facilitation of a dehydration reaction involving HCO3(-) in plasma and the excretion of CO(2) gas from arteriolar ECs.
authors.affiliation: Department of Physiology, School of Medicine, Shinshu University, Matsumoto, Japan.
authors.forename: Yoshiko
authors.initials: Y
authors.lastname: Kawai
authors.forename: Kazuo
authors.initials: K
authors.lastname: Yoshida
authors.forename: Maki
authors.initials: M
authors.lastname: Kaidoh
authors.forename: Yumiko
authors.initials: Y
authors.lastname: Yokoyama
authors.forename: Toshio
authors.initials: T
authors.lastname: Ohhashi
mesh_terms: D015703:Antigens, CD / Q000378:metabolism; D001081:Apyrase / Q000378:metabolism; D002245:Carbon Dioxide / Q000378:metabolism*; D002478:Cells, Cultured; D042783:Endothelial Cells / Q000166:cytology / Q000378:metabolism*; D004730:Endothelium, Vascular / Q000166:cytology* / Q000378:metabolism; D006801:Humans; D008168:Lung / Q000098:blood supply; D025261:Mitochondrial Proton-Translocating ATPases / Q000378:metabolism*; D011651:Pulmonary Artery / Q000166:cytology*; D058472:Receptors, Purinergic P2Y1 / Q000378:metabolism; D033081:Shear Strength
chemical_list: D015703:Antigens, CD; D058472:Receptors, Purinergic P2Y1; D002245:Carbon Dioxide; C474451:F1F0-ATP synthase; D001081:Apyrase; C067869:CD39 antigen; D025261:Mitochondrial Proton-Translocating ATPases