In vivo inhibition of transcellular water channels (aquaporin-1) during acute peritoneal dialysis in rats. Carlsson, Ola, Soren Nielsen, El Rasheid Zakaria, and Bengt Rippe. Departments of Nephrology and Physiology, University of Lund, Sweden
APStracts 3:0346H, 1996.
During peritoneal dialysis (PD) a major portion of the osmotically induced water transport to the peritoneum can be predicted to occur through endothelial water-selective channels. Recently Aquaporin-1 (AQP1) has been recognised as the molecular correlate to such channels. Aquaporins can be inhibited by mercurials. In the present study HgCl2 was locally applied to the peritoneal cavity in rats after short-term tissue fixation, used to protect the tissues from HgCl2 damage. Dianeal 3.86% was employed as dialysis fluid, 125I -albumin (RISA) as an intraperitoneal (IP) volume marker and 51Cr-EDTA (constantly infused, iv.) to assess peritoneal small solute permeability characteristics. Immunocytochemistry and immunoelectron microscopy revealed abundant Aquaporin-1 labeling in capillary endothelium in peritoneal tissues, representing sites for HgCl2 inhibition of water transport. HgCl2 treatment reduced water flow and inhibited the sieving of sodium without causing any untoward changes in microvascular permeability, as compared to fixed control rats, where the peritoneal cavity was exposed to tissue fixation alone. In fixed control rats the mean IP volume (IPV) increased from 20.5 0.15 ml to 25.0 0.52 ml in 60 minutes, whereas in the HgCl2 treated rats the increment was only from 20.7 0.23 ml to 23.5 0.4 ml. In fixed control rats, the dialysate Na+ fell from 135.3 0.97 mM to 131.3 1.72 mM whereas in the HgCl2 treated rats the dialysate Na+ concentration remained unchanged between 0 and 40 minutes, further supporting that water channels had been blocked. Computer simulations of peritoneal transport were compatible with a 66 % inhibition of water flow through aquaporins. The observed HgCl2 inhibition of transcellular water channels strongly indicates a critical role of aquaporins in PD, and provides evidence that water channels are crucial in transendothelial water transport when driven by crystalloid osmosis. 

Received 10 July 1995; accepted in final form 15 April 1996.
APS Manuscript Number H632-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 29 August 1996