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J Physiol Volume 536, Number 1, 133-140, October 1, 2001
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Journal of Physiology (2001), 536.1, pp. 133-140
© Copyright 2001 The Physiological Society

Nitric oxide contracts longitudinal smooth muscle of opossum oesophagus via excitation-contraction coupling


Yong Zhang and William G. Paterson


Gastrointestinal Disease Research Unit and Departments of Medicine and Physiology, Queen's University, Kingston, Ontario, Canada K7L 5G2

  1. The effects of sodium nitroprusside (SNP) and diethylenetriamine/nitric oxide adduct (DETA/NO), putative nitric oxide (NO) donors, on opossum oesophageal longitudinal smooth muscle were investigated using isometric tension and intracellular micro-electrode recordings.
  2. SNP produced concentration-dependent contractions of oesophageal longitudinal smooth muscle with an EC50 of 239.6 ± 78.2 µM (mean ± S.E.M., n = 10). Maximal contraction induced by SNP (1 mM) was about 75.5 ± 8.5 % (n = 10) of the 60 mM KCl-induced contraction. The SNP-induced contraction was resistant to tetrodotoxin (TTX; 1 µM), but abolished by nifedipine (1 µM), as well as by niflumic acid (300 µM) and 9-anthroic acid (9-AC; 1 mM), Ca2+-activated Cl- channel blockers.
  3. DETA/NO at concentrations of 100 and 500 µM induced 83.1 ± 24.4 and 104.1 ± 34.9 % of the 60 mM KCl-induced contraction (n = 4), respectively, which was abolished by nifedipine (1 µM), niflumic acid (300 µM) and 9-AC (1 mM).
  4. Pre-application of 1H-[1,2,4]oxidiazolo[4,3,-alpha]quinoxalin-1-one (ODQ) (10 µM), a guanylate cyclase inhibitor, significantly inhibited the SNP-induced contraction, whereas 8-bromo-cGMP (1 mM), a membrane-permeable analogue of cGMP, mimicked the SNP-induced contraction.
  5. Intracellular recordings revealed that SNP (300 µM) depolarized resting membrane potentials (RMPs) and increased the frequency of spontaneous spike-like action potentials. However, these electrical alterations were eliminated by pretreatment with niflumic acid (300 µM).
  6. These results suggest that NO produces an excitation-contraction coupling in opossum oesophageal longitudinal smooth muscle via a cGMP-dependent signalling pathway. This contraction depends on extracellular Ca2+ entry through activation of L-type Ca2+ channels.



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