Sie befinden Sich nicht im Netzwerk der Universität Paderborn. Der Zugriff auf elektronische Ressourcen ist gegebenenfalls nur via VPN oder Shibboleth (DFN-AAI) möglich. mehr Informationen...
Evidence for active H+ secretion by rat alveolar epithelial cells
Ist Teil von
American journal of physiology. Lung cellular and molecular physiology, 1989-12, Vol.257 (6), p.438-L445
Ort / Verlag
United States
Erscheinungsjahr
1989
Quelle
MEDLINE
Beschreibungen/Notizen
R. L. Lubman, S. I. Danto and E. D. Crandall
Will Rogers Institute Pulmonary Research Program, Cornell University Medical College, New York, New York 10021.
A plasma membrane proton-translocating adenosinetriphosphatase (ATPase) has
been identified in rat alveolar pneumocytes in primary culture using the
pH-sensitive fluorescent probe
2',7'-biscarboxyethyl-5,6-carboxyfluorescein. Intracellular pH (pHi) was
acutely lowered by NH3 prepulse in HCO3(-)-free medium buffered with 6 mM
N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid, and its recovery was
measured thereafter under control conditions, in the presence of amiloride
to inhibit Na(+)-H+ antiport, and in the presence of N-ethylmaleimide
(NEM), a plasma membrane H(+)-ATPase inhibitor. Initial rate of pHi
recovery was reduced by 67% in the presence of amiloride, 52% in the
presence of NEM, and 96% in the presence of both. Recovery was decreased
but not abolished in Na(+)-free buffer, was essentially abolished when NEM
was present in the absence of Na+, and was also abolished by addition of
the metabolic inhibitor KCN in glucose- and Na(+)-free medium. These data
suggest that alveolar epithelial cells possess a plasma membrane
H(+)-ATPase. In Na(+)-containing buffer at pH 7.4, steady-state pHi was
7.50. This value was unaffected by amiloride but decreased to 7.01 in the
presence of NEM, suggesting active H(+)-ATPase and inactive Na(+)-H+
antiport at steady-state pHi. We conclude that this plasma membrane
proton-translocating ATPase in alveolar pneumocytes may be an important
mechanism contributing to regulation of steady-state pHi, recovery from
acute intracellular acidification, and modulation of extracellular alveolar
fluid pH.