Nitric oxide inhibits ACh-induced intracellular calcium oscillations in porcine tracheal smooth muscle

Y. S. Prakash, Mathur S Kannan, Gary C. Sieck

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23 Scopus citations


With real-time confocal microscopy, the effect of three nitric oxide (NO) donors, S-nitroso-N-acetylpenicillamine, S-nitrosoglutathione, and diethylamine NO adduct, on the dynamic intracellular Ca2+ concentration ([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- Bromoguanosine 3',5'-cyclic monophosphate 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 guanosine 3',5'-cyclic monophosphate-dependent mechanisms. After preexposure 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 BAY K 8644. 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.

Original languageEnglish (US)
Pages (from-to)L588-L596
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Issue number4 16-4
StatePublished - Apr 1997


  • acetylcholine
  • airway
  • confocal microscopy
  • fluorescence
  • guanylyl cyclase
  • sarcoplasmic reticulum
  • second messenger


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