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Nitric oxide contracts longitudinal smooth muscle of opossum oesophagus via excitation ‐ contraction coupling
Author(s) -
Zhang Yong,
Paterson William G.
Publication year - 2001
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.2001.00133.x
Subject(s) - niflumic acid , sodium nitroprusside , contraction (grammar) , nitric oxide , chemistry , biophysics , channel blocker , nifedipine , medicine , endocrinology , biochemistry , biology , calcium , organic chemistry
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 EC 50 of 239.6 ± 78.2 μ m (mean ± s.e.m. , n = 10 ). Maximal contraction induced by SNP (1 m m ) was about 75.5 ± 8.5 % ( n = 10 ) of the 60 m m KCl‐induced contraction. The SNP‐induced contraction was resistant to tetrodotoxin (TTX; 1 μ m ), but abolished by nifedipine (1 μ m ), as well as by niflumic acid (300 μ m ) and 9‐anthroic acid (9‐AC; 1 m m ), Ca 2+ ‐activated Cl − channel blockers. 3 DETA/NO at concentrations of 100 and 500 μ m induced 83.1 ± 24.4 and 104.1 ± 34.9 % of the 60 m m KCl‐induced contraction ( n = 4 ), respectively, which was abolished by nifedipine (1 μ m ), niflumic acid (300 μ m ) and 9‐AC (1 m m ). 4 Pre‐application of 1H‐[1,2,4]oxidiazolo[4,3,‐α]quinoxalin‐1‐one (ODQ) (10 μ m ), a guanylate cyclase inhibitor, significantly inhibited the SNP‐induced contraction, whereas 8‐bromo‐cGMP (1 m m ), a membrane‐permeable analogue of cGMP, mimicked the SNP‐induced contraction. 5 Intracellular recordings revealed that SNP (300 μ m ) 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 μ m ). 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 Ca 2+ entry through activation of L‐type Ca 2+ channels.