Vasoconstriction triggered by hydrogen sulfide: Evidence for Na+,K+,2Cl-cotransport and L-type Ca2+ channel-mediated pathway
Objectives: This study examined the dose-dependent actions of hydrogen sulfide donor sodium hydrosulphide (NaHS) on isometric contractions and ion transport in rat aorta smooth muscle cells (SMC). Methods: Isometric contraction was measured in ring aortas segments from male Wistar rats. Activity of...
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| Format: | Article |
| Language: | English |
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Elsevier
2017-12-01
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| Series: | Biochemistry and Biophysics Reports |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S2405580817301243 |
| _version_ | 1819261989707317248 |
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| author | Sergei N. Orlov Svetlana V. Gusakova Liudmila V. Smaglii Svetlana V. Koltsova Svetalana V. Sidorenko |
| author_facet | Sergei N. Orlov Svetlana V. Gusakova Liudmila V. Smaglii Svetlana V. Koltsova Svetalana V. Sidorenko |
| author_sort | Sergei N. Orlov |
| collection | DOAJ |
| description | Objectives: This study examined the dose-dependent actions of hydrogen sulfide donor sodium hydrosulphide (NaHS) on isometric contractions and ion transport in rat aorta smooth muscle cells (SMC).
Methods: Isometric contraction was measured in ring aortas segments from male Wistar rats. Activity of Na+/K+-pump and Na+,K+,2Cl-cotransport was measured in cultured endothelial and smooth muscle cells from the rat aorta as ouabain-sensitive and ouabain-resistant, bumetanide-sensitive components of the 86Rb influx, respectively.
Results: NaHS exhibited the bimodal action on contractions triggered by modest depolarization ([K+]o=30 mM). At 10−4 M, NaHS augmented contractions of intact and endothelium-denuded strips by ~ 15% and 25%, respectively, whereas at concentration of 10−3 M it decreased contractile responses by more than two-fold. Contractions evoked by 10−4 M NaHS were completely abolished by bumetanide, a potent inhibitor of Na+,K+,2Cl-cotransport, whereas the inhibition seen at 10−3 M NaHS was suppressed in the presence of K+ channel blocker TEA. In cultured SMC, 5×10−5 M NaHS increased Na+,K+,2Cl- - cotransport without any effect on the activity of this carrier in endothelial cells. In depolarized SMC, 45Ca influx was enhanced in the presence of 10−4 M NaHS and suppressed under elevation of [NaHS] up to 10−3 M. 45Ca influx triggered by 10−4 M NaHS was abolished by bumetanide and L-type Ca2+ channel blocker nicardipine.
Conclusions: Our results strongly suggest that contractions of rat aortic rings triggered by low doses of NaHS are mediated by activation of Na+,K+,2Cl-cotransport and Ca2+ influx via L-type channels. |
| first_indexed | 2024-12-23T19:50:34Z |
| format | Article |
| id | doaj.art-b9832c96a5ec4df09a99311a46442c79 |
| institution | Directory Open Access Journal |
| issn | 2405-5808 |
| language | English |
| last_indexed | 2024-12-23T19:50:34Z |
| publishDate | 2017-12-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Biochemistry and Biophysics Reports |
| spelling | doaj.art-b9832c96a5ec4df09a99311a46442c792022-12-21T17:33:23ZengElsevierBiochemistry and Biophysics Reports2405-58082017-12-0112C22022710.1016/j.bbrep.2017.09.010Vasoconstriction triggered by hydrogen sulfide: Evidence for Na+,K+,2Cl-cotransport and L-type Ca2+ channel-mediated pathwaySergei N. Orlov0Svetlana V. Gusakova1Liudmila V. Smaglii2Svetlana V. Koltsova3Svetalana V. Sidorenko4Central Research Laboratory, Siberian State Medical University, Moskovskiy trakt 2, Tomsk 634050, RussiaDepartment of Biophysics and Functional Diagnostics, Medical and Biological Faculty, Siberian State Medical University, Moskovskiy trakt 2, Tomsk 634050, RussiaDepartment of Biophysics and Functional Diagnostics, Medical and Biological Faculty, Siberian State Medical University, Moskovskiy trakt 2, Tomsk 634050, RussiaFaculty of Biology MV Lomonosov Moscow State University, Leninskiye gory 1/12, Moscow 119991, RussiaFaculty of Biology MV Lomonosov Moscow State University, Leninskiye gory 1/12, Moscow 119991, RussiaObjectives: This study examined the dose-dependent actions of hydrogen sulfide donor sodium hydrosulphide (NaHS) on isometric contractions and ion transport in rat aorta smooth muscle cells (SMC). Methods: Isometric contraction was measured in ring aortas segments from male Wistar rats. Activity of Na+/K+-pump and Na+,K+,2Cl-cotransport was measured in cultured endothelial and smooth muscle cells from the rat aorta as ouabain-sensitive and ouabain-resistant, bumetanide-sensitive components of the 86Rb influx, respectively. Results: NaHS exhibited the bimodal action on contractions triggered by modest depolarization ([K+]o=30 mM). At 10−4 M, NaHS augmented contractions of intact and endothelium-denuded strips by ~ 15% and 25%, respectively, whereas at concentration of 10−3 M it decreased contractile responses by more than two-fold. Contractions evoked by 10−4 M NaHS were completely abolished by bumetanide, a potent inhibitor of Na+,K+,2Cl-cotransport, whereas the inhibition seen at 10−3 M NaHS was suppressed in the presence of K+ channel blocker TEA. In cultured SMC, 5×10−5 M NaHS increased Na+,K+,2Cl- - cotransport without any effect on the activity of this carrier in endothelial cells. In depolarized SMC, 45Ca influx was enhanced in the presence of 10−4 M NaHS and suppressed under elevation of [NaHS] up to 10−3 M. 45Ca influx triggered by 10−4 M NaHS was abolished by bumetanide and L-type Ca2+ channel blocker nicardipine. Conclusions: Our results strongly suggest that contractions of rat aortic rings triggered by low doses of NaHS are mediated by activation of Na+,K+,2Cl-cotransport and Ca2+ influx via L-type channels.http://www.sciencedirect.com/science/article/pii/S2405580817301243Smooth muscle cellsRat aortaHydrogen sulfideNa+,K+,2Cl-cotransportCa2+ influxContraction |
| spellingShingle | Sergei N. Orlov Svetlana V. Gusakova Liudmila V. Smaglii Svetlana V. Koltsova Svetalana V. Sidorenko Vasoconstriction triggered by hydrogen sulfide: Evidence for Na+,K+,2Cl-cotransport and L-type Ca2+ channel-mediated pathway Biochemistry and Biophysics Reports Smooth muscle cells Rat aorta Hydrogen sulfide Na+,K+,2Cl-cotransport Ca2+ influx Contraction |
| title | Vasoconstriction triggered by hydrogen sulfide: Evidence for Na+,K+,2Cl-cotransport and L-type Ca2+ channel-mediated pathway |
| title_full | Vasoconstriction triggered by hydrogen sulfide: Evidence for Na+,K+,2Cl-cotransport and L-type Ca2+ channel-mediated pathway |
| title_fullStr | Vasoconstriction triggered by hydrogen sulfide: Evidence for Na+,K+,2Cl-cotransport and L-type Ca2+ channel-mediated pathway |
| title_full_unstemmed | Vasoconstriction triggered by hydrogen sulfide: Evidence for Na+,K+,2Cl-cotransport and L-type Ca2+ channel-mediated pathway |
| title_short | Vasoconstriction triggered by hydrogen sulfide: Evidence for Na+,K+,2Cl-cotransport and L-type Ca2+ channel-mediated pathway |
| title_sort | vasoconstriction triggered by hydrogen sulfide evidence for na k 2cl cotransport and l type ca2 channel mediated pathway |
| topic | Smooth muscle cells Rat aorta Hydrogen sulfide Na+,K+,2Cl-cotransport Ca2+ influx Contraction |
| url | http://www.sciencedirect.com/science/article/pii/S2405580817301243 |
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