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A novel alveolar Krebs cycle-triggered CO2 sensing mechanism regulates regional pulmonary ventilation. Nature Precedings
Rainer Kiefmann; Paula Keller; Oliver Tritt; Kai Heckel; Sascha Tank; Martina Kiefmann; Leoni Schulte-Uentrop; Alwin Goetz.
Pulmonary perfusion disorders provoke atelectasis in order to minimize ventilation/perfusion mismatch. However, the underlying mechanisms remain unknown. Because intraalveolar CO2 concentration ([CO2]iA) declines as a consequence of poor pulmonary perfusion we postulated the existence a novel alveolar CO2-sensing mechanism which adapts the ventilation to perfusion. Real-time fluorescence imaging of rat lungs revealed that low [CO2]iA decreased cytosolic and increased mitochondrial Ca2+ in alveolar epithelial cells (AEC), leading to reduction of surfactant secretion and alveolar ventilation. Mitochondrial inhibition by ruthenium red or rotenone blocked the hypocapnia-induced responses. In cultured Type 2 AEC hypocapnia decreased cytosolic Ca2+ independently...
Tipo: Manuscript Palavras-chave: Molecular Cell Biology.
Ano: 2011 URL: http://precedings.nature.com/documents/6185/version/1
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