| pubmed-article:11579163 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11579163 | lifeskim:mentions | umls-concept:C0029115 | lld:lifeskim |
| pubmed-article:11579163 | lifeskim:mentions | umls-concept:C0028128 | lld:lifeskim |
| pubmed-article:11579163 | lifeskim:mentions | umls-concept:C1267092 | lld:lifeskim |
| pubmed-article:11579163 | lifeskim:mentions | umls-concept:C0014876 | lld:lifeskim |
| pubmed-article:11579163 | lifeskim:mentions | umls-concept:C0205127 | lld:lifeskim |
| pubmed-article:11579163 | lifeskim:mentions | umls-concept:C0332522 | lld:lifeskim |
| pubmed-article:11579163 | lifeskim:mentions | umls-concept:C1948027 | lld:lifeskim |
| pubmed-article:11579163 | pubmed:issue | Pt 1 | lld:pubmed |
| pubmed-article:11579163 | pubmed:dateCreated | 2001-10-1 | lld:pubmed |
| pubmed-article:11579163 | pubmed:abstractText | 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 microM (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 microM), but abolished by nifedipine (1 microM), as well as by niflumic acid (300 microM) and 9-anthroic acid (9-AC; 1 mM), Ca(2+)-activated Cl(-) channel blockers. 3. DETA/NO at concentrations of 100 and 500 microM 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 microM), niflumic acid (300 microM) and 9-AC (1 mM). 4. Pre-application of 1H-[1,2,4]oxidiazolo[4,3,-alpha]quinoxalin-1-one (ODQ) (10 microM), 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 microM) 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 microM). 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. | lld:pubmed |
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| pubmed-article:11579163 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:11579163 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:11579163 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11579163 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:11579163 | pubmed:issn | 0022-3751 | lld:pubmed |
| pubmed-article:11579163 | pubmed:author | pubmed-author:PatersonW GWG | lld:pubmed |
| pubmed-article:11579163 | pubmed:author | pubmed-author:ZhangYY | lld:pubmed |
| pubmed-article:11579163 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11579163 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:11579163 | pubmed:volume | 536 | lld:pubmed |
| pubmed-article:11579163 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11579163 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11579163 | pubmed:pagination | 133-40 | lld:pubmed |
| pubmed-article:11579163 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:11579163 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11579163 | pubmed:articleTitle | Nitric oxide contracts longitudinal smooth muscle of opossum oesophagus via excitation-contraction coupling. | lld:pubmed |
| pubmed-article:11579163 | pubmed:affiliation | Gastrointestinal Disease Research Unit and Departments of Medicine and Physiology, Queen's University, Kingston, Ontario, Canada K7L 5G2. | lld:pubmed |
| pubmed-article:11579163 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11579163 | pubmed:publicationType | In Vitro | lld:pubmed |
| pubmed-article:11579163 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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