Neuroendocrine and metabolic factors in pulmonary circulatory control.
New approaches to elucidating control mechanisms of the pulmonary circulation are presented. The relationship of inspired oxygen, pulmonary arterial medial thickness, numbers, and serotonin fluorescence intensity of pulmonary neuroendocrine cells is described. Neuroendocrine cells appear to react to changes in O2 level by a decrease in serotonin emission intensity acutely and chronically. The response of the cell numbers is different between acute hypoxic and hyperoxic exposure but similar under chronic exposure conditions. The roles of neither serotonin nor the regulatory peptides localized in the lung are defined; however, a possible relationship between these elements is described. Although Weir's hypothesis of normoxic pulmonary vasodilatation is compatible with these concepts, evidence for its proof is still lacking.
D001078:APUD Cells / Q000166:cytology / Q000378:metabolism*; D000818:Animals; D001839:Bombesin / Q000378:metabolism; D002452:Cell Count; D005246:Feedback; D000860:Hypoxia / Q000503:physiopathology; D008168:Lung / Q000166:cytology / Q000196:embryology; D010101:Oxygen Consumption; D011652:Pulmonary Circulation; D011817:Rabbits; D012701:Serotonin / Q000378:metabolism; D013373:Substance P / Q000378:metabolism
D012701:Serotonin; D013373:Substance P; D001839:Bombesin