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.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.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).Pre-application of 1H-[1,2,4]oxidiazolo[4,3,-α]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.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).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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