Hypoxia impairs nitrovasodilator-induced pulmonary vasodilation:
role of na-k-adenosine triphosphatase activity.
Tamaoki, Jun, Etsuko Tagaya, Isao Yamawaki, and Kimio Konno.
First Department of Medicine, Tokyo Women's Medical College, Tokyo
162, Japan
APStracts 3:0037L, 1996.
To elucidate the effect of hypoxia on nitrovasodilator-induced
pulmonary vasodilation, we studied canine pulmonary arterial rings
under isometric conditions in vitro. Exposure to hypoxia inhibited
the relaxant responses of KCl-contracted tissues to sodium
nitroprusside (SNP), so that the maximal relaxation (Emax) and the
negative logarithm of molar concentration required to produce 50%
relaxation (pD2) were decreased from 92 +/- 7 to 62 +/- 5% and from
5.8 +/- 0.2 to 4.7 +/- 0.3, respectively (means +/- SE, P < 0.01
for each). This effect was likewise observed when 8-bromo-cGMP was
used as a relaxant. The impairment of SNP-induced relaxation of
endothelium-denuded rings under hypoxia was abolished by ouabain or
K+-free solution. Incubation with SNP dose-dependently increased
intracellular cGMP contents, an effect that was not altered by
hypoxia. SNP also increased ouabain-sensitive 86Rb-uptake, and this
effect was inhibited by hypoxia. These results suggest that hypoxia
reduces nitrovasodilator-induced relaxation of pulmonary artery
probably through an inhibition of cGMP-dependent sarcolemmal Na-K
-adenosine triphosphatase activity.
Received 7 August 1995; accepted in final form 3 March 1996.
APS Manuscript Number L248-5.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 20 March 96