Journal of Applied Physiology, Vol 74, Issue 1 111-115, Copyright © 1993 by American Physiological Society

ARTICLES

Amiloride blocks the inhibition of fetal lung liquid secretion caused by AVP but not by asphyxia

S. B. Hooper, M. J. Wallace and R. Harding
Department of Physiology, Monash University, Clayton, Victoria, Australia.

We have examined whether the activation of Na+ channels, located on the luminal surface of pulmonary epithelial cells, mediates the inhibitory effects of both arginine vasopressin (AVP) and moderate asphyxia on fetal lung liquid secretion. Lung liquid secretion rates were measured in chronically catheterized fetal sheep during AVP infusions and during periods of asphyxia with and without an Na+ transport blocker (amiloride; 10(-4) M) present in lung liquid. Lung liquid secretion rates were also measured during epinephrine infusions with amiloride present in lung liquid. These secretion rates were compared with measurements made during a preceding control period. Both asphyxia and an infusion of AVP significantly reduced the rate of secretion of fetal lung liquid from 8.4 +/- 1.5 and 18.0 +/- 3.7 to 3.6 +/- 1.0 (P < 0.01) and 5.5 +/- 2.1 ml/h (P < 0.01), respectively. The addition of amiloride to lung liquid did not reverse the inhibitory effects of asphyxia on lung liquid secretion (8.6 +/- 0.8 vs. 0.7 +/- 0.4 ml/h) but did block the inhibitory effects of both epinephrine (14.8 +/- 4.4 vs. 13.8 +/- 3.1 ml/h) and AVP (18.0 +/- 3.7 vs. 19.5 +/- 5.0 ml/h). The addition of amiloride to lung liquid during fetal normoxia did not significantly affect fetal lung liquid secretion rates (8.2 +/- 1.1 vs. 7.4 +/- 0.7 ml/h). We conclude that the inhibitory effect of AVP on fetal lung liquid secretion, like that of epinephrine, involves the activation of luminal surface Na+ channels, whereas the inhibitory effect of asphyxia does not.

This article has been cited by other articles:

				C. Nicco, M. Wittner, A. DiStefano, S. Jounier, L. Bankir, and N. Bouby Chronic Exposure to Vasopressin Upregulates ENaC and Sodium Transport in the Rat Renal Collecting Duct and Lung Hypertension, November 1, 2001; 38(5): 1143 - 1149. [Abstract] [Full Text] [PDF]

				L. Bankir Antidiuretic action of vasopressin: quantitative aspects and interaction between V1a and V2 receptor-mediated effects Cardiovasc Res, August 15, 2001; 51(3): 372 - 390. [Abstract] [Full Text] [PDF]

				B. Pouzet, C. Serradeil-Le Gal, N. Bouby, J.-P. Maffrand, G. Le Fur, and L. Bankir Selective blockade of vasopressin V2 receptors reveals significant V2-mediated water reabsorption in Brattleboro rats with diabetes insipidus Nephrol. Dial. Transplant., April 1, 2001; 16(4): 725 - 734. [Abstract] [Full Text] [PDF]

				A. Lines, S. B. Hooper, and R. Harding Lung liquid production rates and volumes do not decrease before labor in healthy fetal sheep J Appl Physiol, March 1, 1997; 82(3): 927 - 932. [Abstract] [Full Text] [PDF]

				O. A. Itani, S. D. Auerbach, R. F. Husted, K. A. Volk, S. Ageloff, M. A. Knepper, J. B. Stokes, and C. P. Thomas Alveolar Epithelial Ion and Fluid Transport: Glucocorticoid-stimulated lung epithelial Na+ transport is associated with regulated ENaC and sgk1 expression Am J Physiol Lung Cell Mol Physiol, April 1, 2002; 282(4): L631 - L641. [Abstract] [Full Text] [PDF]