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J Appl Physiol 83: 1002-1016, 1997;
8750-7587/97 $5.00
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Journal of Applied Physiology
Vol. 83, No. 3, pp. 1002-1016, September 1997
PULMONARY CIRCULATION AND LUNG FLUID BALANCE

Water transport and the distribution of aquaporin-1 in pulmonary air spaces

R. M. Effros1, C. Darin1, E. R. Jacobs1, R. A. Rogers2, G. Krenz3, and E. E. Schneeberger4

1 Division of Pulmonary and Critical Care Medicine, Department of Medicine, and 3 Human Physiology Laboratory, Medical College of Wisconsin, Milwaukee, Wisconsin 53226; 2 Physiology Program, Harvard School of Public Health, Boston 02115; and 4 Department of Pathology, Massachusetts General Hospital, Boston, Massachusetts 02114

Received 7 May 1996; accepted in final form 1 April 1997.

Effros, R. M., C. Darin, E. R. Jacobs, R. A. Rogers, G. Krenz, and E. E. Schneeberger. Water transport and the distribution of aquaporin-1 in pulmonary air spaces. J. Appl. Physiol. 83(3): 1002-1016, 1997.---Recent evidence suggests that water transport between the pulmonary vasculature and air spaces can be inhibited by HgCl2, an agent that inhibits water channels (aquaporin-1 and -5) of cell membranes. In the present study of isolated rat lungs, clearances of labeled (3HOH) and unlabeled water were compared after instillation of hypotonic or hypertonic solutions into the air spaces or injection of a hypotonic bolus into the pulmonary artery. The clearance of 3HOH between the air spaces and perfusate after intratracheal instillation and from the vasculature to the tissues after pulmonary arterial injections was invariably greater than that of unlabeled water, indicating that osmotically driven transport of water is limited by permeability of the tissue barriers rather than the rate of perfusion. Exposure to 0.5 mM HgCl2 in the perfusate and air-space solution reduced the product of the filtration coefficient and surface area (PfS) of water from the air spaces to the perfusate by 28% after instillation of water into the trachea. In contrast, perfusion of 0.5 mM HgCl2 in air-filled lungs reduced PfS of the endothelium by 86% after injections into the pulmonary artery, suggesting that much of the action of this inhibitor is on the endothelial surfaces. Confocal laser scanning microscopy demonstrated that aquaporin-1 is on mouse pulmonary endothelium. No aquaporin-1 was found on alveolar type I cells with immunogold transmission electron microscopy, but small amounts were present on some type II cells.

28-kDa channel-forming integral membrane protein; mercuric chloride; epithelium; endothelium; immunogold

0161-7567/97 $5.00 Copyright © 1997 the American Physiological Society




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