Airways of a hyperresponsive rat strain show decreased relaxant
responses to sodium nitroprusside.
Jia, Yanlin, Lijing Xu, Seymour Heisler, and James G. Martin.
Meakins-Christie Laboratories, McGill University and Cystic
Fibrosis Laboratory, Montreal Chest Hospital, Montreal, Quebec,
Canada H2X 2P2
APStracts 2:0045L, 1995.
The aim of the current studies was to investigate the possibility that
a decreased relaxant response to nitric oxide (NO) might contribute
to strain-related differences in airway responsiveness in the rat.
Isolated tracheal rings from hyperresponsive Fisher rats were
confirmed to be more responsive to carbachol (EC50=2.45x10-7M) than
those from Lewis (EC50=3.60x10-7M, p<0.03) and ACI (EC50=3.85x10
-7M, p<0.01) rats. Sodium nitroprusside (SNP), a NO donor, caused
relaxation of the carbachol (10-6M) contracted tracheal rings but the
IC50 SNP in Fisher rats (5.60x10-6M) was significantly higher than
that in Lewis (1.34x10-6M, p<0.001) and ACI rats (1.13x10-6M,
p<0.0005). The inhibitory effect of SNP on airway responsiveness to
inhaled methacholine (MCh) in vivo was also less pronounced for
Fisher than Lewis rats. SNP induced an accumulation of cyclic GMP in
cultured tracheal smooth muscle cells (TSM). Fisher TSM produced less
cyclic GMP on exposure to SNP compared with ACI (p<0.01) and Lewis
(p<0.0001). A decreased guanylyl cyclase activity may account for
the impaired relaxant effect of SNP in Fisher rats.
Received 18 July 1994; accepted in final form 22 March 1995.
APS Manuscript Number L200-4.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 4 April 1995.