Nitric oxide inhibits acetylcholine-induced intracellular calcium
oscillations in porcine tracheal smooth muscle.
Prakash, Y. S., Mathur S. Kannan, and Gary C. Sieck.
Departments of Anesthesiology, and Physiology & Biophysics, Mayo
Foundation, Rochester, MN 55905, Department of Veterinary
PathoBiology and Pediatrics, University of Minnesota, St. Paul, MN
55108
APStracts 3:0220L, 1996.
Using real-time confocal microscopy, the effect of three nitric oxide
(NO) donors, s-nitroso-n-acetylpenicillamine (SNAP), s
-nitrosoglutathione (GSNO) and diethylamine NO adduct (DEANO) on the
dynamic intracellular Ca2& ([Ca2&]i) response of porcine
tracheal smooth muscle (TSM) cells to acetylcholine (ACh) was
examined. ACh initiated propagating [Ca2&]i oscillations in TSM
cells, which were inhibited by NO donors. 8-bromo-cGMP slowed the
frequency of [Ca2&]i oscillations, but did not completely inhibit
oscillations, suggesting that the effects of NO donors are only
partially mediated via cGMP-dependent mechanisms. After pre-exposure
to NO donors, ACh induced a small, biphasic [Ca2&]i response that
was blocked by nifedipine, suggesting a lack of effect on Ca2&
influx through voltage-gated channels. In addition, NO donors did not
inhibit Ca2& influx induced by BayK8644. The [Ca2&]i response
to caffeine was inhibited by NO donors, indicating inhibition of
sarcoplasmic reticulum (SR) Ca2& release. When Ca2& influx
and SR Ca2& reuptake were blocked, basal [Ca2&]i increased,
and this was inhibited by NO donors, suggesting enhanced Ca2&
efflux. These results indicate that NO donors inhibit [Ca2&]i
oscillations by blocking SR Ca2& release and enhancing Ca2&
extrusion.
Received 16 June 1996; accepted in final form 31 October 1996.
APS Manuscript Number L167-6.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 31 December 1996