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1 CIHR Group in Lung Development, The Hospital for Sick Children, Toronto, Canada; Physiology and Experimental Medicine, The Hospital for Sick Children , Toronto, Canada; Physiology, The University of Toronto, Toronto, Canada
2 CIHR Group in Lung Development, The Hospital for Sick Children, Toronto, Canada; Physiology and Experimental Medicine, The Hospital for Sick Children , Toronto, Canada
3 CIHR Group in Lung Development, The Hospital for Sick Children , Toronto, Canada; Physiology and Experimental Medicine, The Hospital for Sick Children , Toronto, Canada
4 Genetics and Genome Biology, The Hospital for Sick Children, Toronto, Canada; Laboratory Medicine and Pathobiology, The University of Toronto, Toronto, Canada
5 Physiology, Emory University, Atlanta, Georgia, United States
6 Pediatrics, Emory University, Atlanta, Georgia, United States
7 CIHR Group in Lung Development, The Hospital for Sick Children, Toronto, Canada; Physiology and Experimental Medicine, The Hospital for Sick Children , Toronto, Canada; Paediatrics, The University of Toronto, Toronto, Canada
8 CIHR Group in Lung Development, The Hospital for Sick Children, Toronto, Canada; Physiology and Experimental Medicine, The Hospital for Sick Children , Toronto, Canada; Physiology, The University of Toronto, Toronto, Canada; Paediatrics, The University of Toronto, Toronto, Canada
* To whom correspondence should be addressed. E-mail: hugh.obrodovich{at}sickkids.ca.
We have previously shown that cardiogenic pulmonary edema fluid (EF) increases Na+ and fluid transport by fetal distal lung epithelia (FDLE) (Rafii et al, J. Physiol 2002). We now report the effect of EF on Na+ and fluid transport by the adult lung. We first studied primary cultures of adult type II (ATII) epithelium and found that overnight exposure to EF increased Na+ transport, and this effect is mainly due to factors other than catecholamines. Plasma did not stimulate Na+ transport in ATII. Purification of EF demonstrated that at least some agent(s) responsible for the amiloride-insensitive component resided within the globulin fraction. ATII exposed to globulins demonstrated a conversion of amiloride-sensitive short circuit current (Isc) to amiloride-insensitive Isc with no increase in total Isc. Patch clamp studies showed that ATII exposed to EF for 18h had increased the number of highly selective Na+ channels in their apical membrane. In situ acute exposure to EF increased the open probability of Na+ permeant ion channels in ATII within rat lung slices. EF did increase, by amiloride-sensitive pathways, the alveolar fluid clearance from the lungs of adult rats. We conclude that cardiogenic EF increases Na+ transport by adult lung epithelia in primary cell culture, in situ, and in vivo.
This article has been cited by other articles:
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  H. O'Brodovich, P. Yang, S. Gandhi, and G. Otulakowski Amiloride-insensitive Na+ and fluid absorption in the mammalian distal lung Am J Physiol Lung Cell Mol Physiol, March 1, 2008; 294(3): L401 - L408. [Abstract] [Full Text] [PDF]
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