Nitric oxide inhibits calcium release from the sarcoplasmic
reticulum of porcine tracheal smooth muscle cells.
Kannan, Mathur S., Y. S. Prakash, Dana E. Johnson, and Gary C. Sieck.
Departments of Veterinary PathoBiology and Pediatrics, University
of Minnesota, St. Paul, MN 55108 and Departments of Anesthesiology,
and Physiology & Biophysics, Mayo Foundation, Rochester, MN
55905
APStracts 3:0143L, 1996.
In the present study, effects of the nitric oxide (NO) donor, s
-nitroso-n-acetylpenicillamine (SNAP), on sarcoplasmic reticulum (SR)
Ca2+ release were examined in freshly-dissociated porcine tracheal
smooth muscle (TSM) cells. Fura 2-loaded TSM cells were imaged using
video fluorescence microscopy. SR Ca2+ release was induced by
acetylcholine (ACh), which acts principally through inositol 1,4,5
-trisphosphate (IP3) receptors, and by caffeine, which acts
principally through ryanodine receptors (RyR). SNAP inhibited ACh
-induced SR Ca2+ release at both zero and 2.5 mM extracellular Ca2+.
Degraded SNAP had no effect on ACh-induced SR Ca2+ release. SNAP also
inhibited caffeine-induced SR Ca2+ release. ACh-induced Ca2+ influx
was not affected by SNAP, when SR reloading was blocked by
thapsigargin. SNAP also did not affect SR Ca2+ reuptake. The
membrane-permeant analog of cGMP, 8-bromo-cGMP, mimicked the effects
of SNAP. These results suggest that, in porcine TSM cells, SNAP
reduces the intracellular Ca2+ response to ACh and caffeine by
inhibiting SR Ca2+ release through both IP3 and RyR, but not by
inhibiting influx or repletion of the SR Ca2+ stores. These effects
are likely mediated via cGMP-dependent mechanisms.
Received 18 March 1996; accepted in final form 20 August 1996.
APS Manuscript Number L85-6.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 19 September 1996